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Cancer 3 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

3 components of fighting against cancer

A
  1. Prevention ⇒ such as avoiding carcinogens
  2. Early diagnosis ⇒ the earlier it is found the easier it is to treat
  3. Treatment
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2
Q

why are mutations bad but still important?

A

important for our cells and evolutionary drive

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3
Q

how much of cancer is attributed to modifiable risk?

A

40%
- cigarette smoking
- excess body weight
- Alcohol
- UV
- inactivity
- etc.

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4
Q

how do cell errors eventually cause cancer?

A

errors in DNA replication accumulate each time a cell divides
- Eventually enough of these mutations occur in checkpoints or repair mechanisms that cells become cancerous

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5
Q

there is a positive correlation between step cell divisions and what?

A

incidence of cancer in a certain cell type
- a significant component of cancer risk is inherent and due to bad luck through these accumulated mutations

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6
Q

what are highly environmental cancers?

A

Mesothelioma (asbestos exposure), lung cancer (smoking), cervical cancer (HPV)

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7
Q

Medium environmental ⇒ risk is increased by environmental factors but also driven by intrinsic risk

A

Colorectal carcinoma, breast cancer, pancreatic cancer

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8
Q

Low environmental impact ⇒ mostly intrinsic in nature

A

Prostate cancer, brain cancer, non hodgkin’s lymphoma

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9
Q

Least environmental impact ⇒ hereditary or genetic in nature

A

Retinoblastoma, pediatric neuroblastoma, acute lymphoblastic leukemia

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10
Q

what is a 3rd component of cancer?

A

hereditary mutations can increase your risk of developing cancer

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11
Q

Li Fraumeni syndrome

A

inherited mutations in P53 leading to increased risk of all cancers

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12
Q

BRCa2 deficiency

A

mutations in a tumor suppressor gene are increased risk of breast and ovarian cancer

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13
Q

how does heterozygosity work for tumor suppressor genes?

A

if the remaining ones become mutated will lead to cancer
- Should be reviewed by genetic counselors to figure out variants in genomes

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14
Q

what environmental effects affect cancer? (3)

A
  1. Carcinogen activation
  2. Ionizing radiation
  3. UV radiation
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15
Q

what is carcinogen activation; most potent carcinogens?

A

a few carcinogens act directly on DNA and the most potent carcinogens are initially chemically inert and only becoming damaging after metabolic processes in the liver

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16
Q

Cytochrome P-450 oxidases

A

normally convert toxins into harmless molecules but certain chemicals can be converted to highly mutagenic products

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17
Q

how do aflatoxin and cytochrome P-450 interact?

A

aflatoxin derived from mold that grows on grains and peanuts when stored under humid tropical conditions and cytochrome P-450 can catalyze aflatoxin B1 to aflatoxin 2-3 epoxide to become a carcinogen in DNA

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18
Q

ionizing radiation and components (5)

A

x-rays and other scans can directly affect DNA and can generate reactive oxygen species
- Cross linking
- Breaks
- Base modifications
- May directly affect DNA
- Can drive oncogenic processes ⇒ migration, invasion, angiogenesis

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19
Q

UV radiation and components (3)

A

induces formation of pyrimidine (cytosine and thymine) dimers so they link together on the same strand and is a significant risk factor for developing melanoma
- Causes crosslinking between bases and distorts the DNA double helix
- Interferes with polymerases generating errors in transcription and replication
- Primarily resolved through nucleotide excision repair

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20
Q

how is inflammation involved in cancer?

A

inflammation is pro-oncogenic

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21
Q

what % of cancer is oncoviruses responsible for; what are examples?

A

20%
1. direct
- Epstein barr virus
- Human papillomavirus
- Human T-lymphotropic virus
2. indirectly
- Hepatitis B and C

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22
Q

Human papillomavirus (HPV)

A

primary cause of uterine cervix carcinoma and agent of genital warts
- Infection usually lasts approximately 2 years
- Highly effective vaccine available => referred to as a cancer vaccine

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23
Q

how does HPV work?

A

infects the basal layers of cervical epithelial cells
- Maintained in latent phase as extra chromosomal plastids ⇒ stays with the DNA
- Produce infectious progeny in the outer layer of epithelial cells
- Express proteins that interfere with cell cycle arrest of the host cell in outer layer ⇒ excess proliferation of cells
- This produces benign warts that allow release of viral progeny and spread of the disease

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24
Q

what does the presence of the extra chromosomal DNA lead to in HPV?

A

integration into the host genome via recombination ⇒ break in host genome and homologous recombination occurs
- This can lead to uncontrolled production of viral proteins in the basal layer cells ⇒ mitotic cells
- These genes act as oncogenes ⇒ directly leading to oncogenesis and proliferation

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25
Q

what is integration in the basal layer a problem?

A

it will express proteins responsible for cell growth and result in invasion from the epithelial layer leading to cervical cancer

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26
Q

Adult T-cell lymphoma virus type 1

A

human retrovirus that infects lymphocytes with a lifelong infection ⇒ normally asymptomatic
- 5% of infected individuals will develop adult t-cell lymphoma
- Transmission occurs through breast milk, sexual contact, intravenous drug use (needle sharing)

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27
Q

how does TLV-1 oncogenesis work?

A

viral proteins directly interfere with processes to favor and maintain viral infection and persistence as a retrovirus
- Much of this has been traced to the viral oncogene Tax

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28
Q

Tax

A

a viral oncogene that interferes with cell processes so the virus maintained and spreads

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29
Q

components of Tax (3)

A
  • Dysregulation of cell cycle
  • Inhibition of apoptosis
  • Alterations in gene expression
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30
Q

Epstein-Barr virus (EBV)

A

causative agent of mononucleosis (mono)
- Vast majority of individuals will experience a 4-6 week infection or no symptoms at all
- 90% + of adults exposed
- Infection is lifelong, virus remains dormant in tissues and can become reactivated in times of stress, infection, or immunocompromised

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31
Q

how does EBV cause cancer

A

EBV can cause cancer in multiple tissue types
- EBV viral genes are directly oncogenic
ex: Burkitt’s lymphoma

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32
Q

EBNA1

A

viral protein binds to host genome on chromosome 11
- Region has homology to EBV genome
- Binding leads to double stranded breaks in a region responsible for regulating cell growth
- Induces rearrangement to stimulate Myc expression

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33
Q

Hepatitis B/C

A

chronic infections that lead to chronic liver inflammation and eventually cirrhosis
- Hepat: liver
- Itis: inflammation of
- lifelong infections, controllable with medication but incurable ⇒ vaccine available for B but not C

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34
Q

how can Hep B and C cause cancer?

A

hepatitis B and C can cause cancer through indirect mechanisms but not through integration of expression of viral oncogenes
- The sustained damaging and inflammatory environment promotes tumor growth
- Damage to cells leads to DNA damage and mutations
- Inflammation triggers healing and cell growth, immunosuppression, angiogenesis
- Proper treatment limits risk of oncogenesis

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35
Q

what are available effective vaccines

A
  • Hepatitis B
  • HPV
  • Others under development
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36
Q

what is the mainstay of curative cancer treatment?

A

surgical resection followed by chemotherapy

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37
Q

requirements of surgical resection? What type of cancers have become increasingly treatable?

A

This requires early diagnosis before metastasis has occurred
- Blood cancers have become increasingly treatable and curable
- early diagnosis and treatment is strongly correlated with favorable outcomes

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38
Q

4 cancers with regular screening guidelines

A
  • Breast
  • Cervical
  • Colorectal
  • Lung
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39
Q

what percent of cancers don’t have a screening test?

A

57%
typically found in patients who are symptomatic which may be indicative of late stage disease

40
Q

what are methods of detection? (3)

A
  • screening
  • molecular markers
  • imaging
41
Q

screening types (3)

A
  • Colonoscopy
  • Physical examination
  • Mammography
42
Q

molecular markers (2)

A
  • Overexpression of certain proteins ⇒ PSA in prostate cancer
  • Blood and fecal tests
43
Q

imaging types (3)

A
  • X-ray
  • MRI
  • Contrast tomography (CT)
44
Q

Positron emission tomography (PET)

A

scan commonly used to identify and track cancerous lesions
- Utilizes radioactively labeled molecules to highlight regions of the body (glucose)

45
Q

Warburg effect

A

cancer cells use aerobic glycolysis even when oxygen is abundant from mTOR activation
- Consume large amounts of glucose
- Regions with high metabolic activity light up in a PET scan

46
Q

is there too much screening

A

there is such a thing as too much screening and overdiagnosis

47
Q

Contrast

A

how much a given therapy affects cancerous cells vs healthy cells

48
Q

3 types of treatments

A
  1. primary treatments
  2. adjacent therapy
  3. palliative care
49
Q

Primary treatment

A

completely remove cancer from your body and kill all cancer cells

50
Q

Adjuvant therapy

A

kill any cancer cells remaining after treatment ⇒ or neo before the primary treatment

51
Q

Palliative care

A

to relieve and improve QOL without curative intent

52
Q

what cancers tend to be highly treatable

A

Early stage and blood cancers
- Metastatic or unresectable solid tumors much less so

53
Q

how does survival work with cancer therapy?

A
  • Overall survival ⇒ % survival over a time frame
  • Progression free survival
54
Q

response related endpoints for measuring cancer therapy

A
  • Tumor volume reduction
  • Cure fraction
55
Q

cure fraction

A

the proportion of patients that survive due to the treatment therapy over an extended period of time

56
Q

traditional therapies

A
  1. surgical resection
  2. radiation
  3. chemotherapy
57
Q

surgical resection; what does removing a tumor do?

A

involves the removal of cancerous tissue
- Often only beneficial to overall survival if the tumor is not yet metastatic or if metastases are responding well to treatment
- removal of a tumor may take away your body’s antitumor ability by taking out the main tumor ⇒ it will not fight against the rest of the metastasis in the body

58
Q

what is needed for surgical resection (2)

A
  • Accessible
  • not spread to critical areas
59
Q

radiation

A

cancer cells often have defective repair mechanisms, they are generally more susceptible to radiation induced DNA damage than healthy cells

60
Q

what are negative effects of radiation?

A
  • Increases the risk of secondary malignancies from treatment itself which induces a second cancer type
  • Tumor must be accessible to radiation
61
Q

what are benefits to radiation?

A
  • Cancer either directly or indirectly kills cells or induces antitumor immunity or apoptosis
  • can be effective as adjunct therapy or for tumors that are not resectable
62
Q

chemotherapy

A

non-specific cytotoxic drugs that target various aspects of cell growth and homeostasis
- Generally function under the principle that cancer cells will be more affected by the effects than healthy cells

63
Q

components of chemotherapy? (2)

A
  • Often rapidly dividing cells are often affected
  • Dosing is limited by systemic toxicity
64
Q

classes of chemotherapy drugs? (4)

A
  1. Alkylating agents
  2. Anti-metabolites
  3. Plant alkaloids
  4. Antitumor antibiotics
65
Q

Alkylating agents

A

attach alkyl groups to DNA interfering with replication and transcription

66
Q

Anti-metabolites

A

substitute for nucleotides, interfere with replication and transcription

67
Q

Plant alkaloids

A

inhibit mitosis ⇒ microtubule formation in taxanes

68
Q

Antitumor antibiotics

A

bind to DNA and inhibit transcription, cause fragmentation

69
Q

Paclitaxel

A

taxmen that stabilize microtubules preventing their degradation
- Stabilizes GTP bound tubulin
- Inhibits chromosome segregation during M-phase
- Triggers mitotic spindle checkpoint

70
Q

what is the class of Paclitaxel?

A

plant alkaloid, mitotic inhibitor

71
Q

Spindle assembly checkpoint

A

unattached kinetochores causes ubiquitinated cyclin B1 and you cannot proceed through M phase
- The cell will return to G1 or it will goto mitotic exit
- sometimes it will try to redo the process but this won’t work

72
Q

5-fluouracil

A

Pyrimidine analog of uracil and Inhibits thymidylate synthetase
- Starves cell of thymine needed for replication
- Secondarily substitutes for uracil in mRNA and thymine in DNA interfering with transcription, translation, replication

73
Q

what class if 5-flurouracil

A

antimetabolite

74
Q

what is the 5-FU mechanism of action?

A

Ends up with low thymine and you can no longer replicate the genome to fill in the T spots

75
Q

Targeted therapies

A

can target cancer cells directly but often require identifications of specific mutations ⇒ sequence, find mutations, analyze lifestyle factors, etc.
- non specific therapies have limited contrast and high systemic toxicity

76
Q

target therapies (6)

A
  • Hormonal
  • Antibody drug conjugates
  • Immunotherapy
  • CarT cell therapy
  • Oncolytic viral therapy
  • Small molecules
77
Q

Small molecules

A

drugs that specifically target cancerous cells but spare healthy cells ⇒ inhibit specific molecules of a pathway specifically dysfunctional in a certain cancer type
- This leads to higher potency and lower toxicity than traditional chemotherapies

78
Q

what are small molecule applicabilities?

A

these are less broadly applicable to all cancers and tend to work on specific types, tend to be highly effective in some patients and ineffective in others
- Can also be conjugated to antibodies to enhance targeting, useful for cell surface markers
- more useful for doing stuff in a cell than antibodies which target the surface

79
Q

immunotherapies

A

seek to either use immune system components to directly target cancer cells or to stimulate the hosts anti-tumor immunity
- Antibodies targeted to cancer antigens can inhibit cancer signaling or trigger elimination
- molecules/receptors overexpressed in cancer will be targeted

80
Q

what can certain cancer mutations do in regards to the immune system?

A

evade immune surveillance

81
Q

what is the early stage breast cancer driver?

A

estrogen receptor signaling
- Estrogen freely diffuses the cell and binds to the estrogen receptor in the cytoplasm
- Complex translocates to the nucleus where it binds to the estrogen response element leading to cell growth and proliferation

82
Q

Tamoxifen

A

specifically binds to the estrogen receptor in breast tissue
- Prevents estrogen from binding and activating transcription
- Estrogen signaling in other tissues remains active
- Highly effective treatment for breast cancer so long as other mutations do not arise
- inhibits co-activator in breast tissue specifically

83
Q

Ras-Mapk pathway & mutations

A

RTK signaling activates Ras and GTP bound form is active
- at some point GTP is removed and ras is inactivated
- Results in downstream signaling that promotes survival and proliferation
- Mutations in Ras can prevent GTP from being hydrolyzed rendering Ras permanently active ⇒ doesn’t require RTK signaling
- Ras activates Raf activates Mek activates Erk/MapK

84
Q

drugs ending in nib are what?

A

small molecule inhibitors

85
Q

drugs ending in mab are what?

A

antibodies

86
Q

why is Ras difficult to inhibit?

A

its affinity for GTP is very high so GTP will always bind instead of a different molecule
- It doesn’t have many grooves for binding to Ras

87
Q

small molecule inhibitor targets in the ras pathway(3)

A
  • Raf inhibitors ⇒ mostly small molecule inhibitors
  • Mek ⇒ mostly small molecule inhibitors
  • RTK ⇒ mix of small molecule inhibitors and antibody techniques
88
Q

are cyclin dependent kinases functional in cancer?

A

often dysfunctional in cancer and become overactive
- CDKs regulate cell cycle progression
- Often dysfunctional in cancer

89
Q

what are effective inhibitors for CDKs

A

Small molecule inhibitors are effective for certain cancers by preventing progression through the cell cycle

90
Q

why is p53 a problematic target?

A

At first glance appears a prime target for molecular therapies but much more difficult to correct a nonfunctional protein than to inhibit an overactive one
- Inhibiting p53 would make the problem even worse

91
Q

what are advanced car-T therapies

A
  1. Car-T cell therapy
  2. Oncolytic viral therapy
92
Q

Car-T cell therapy

A

chimeric antigen receptor T-cells ⇒ engineered T cells that can target specific antigens
- Can be engineered to target tumor antigens
- Highly specific and extremely potent

93
Q

what are downsides of Car-T cell therapy?

A
  • Extreme potency may limit practical applications via targeting of non cancerous cells that express low levels of the same markers
  • Extremely expensive to administer
  • can be problematic because there are no breaks once these are released
94
Q

oncolytic viral therapy

A

utilizes viruses to target cancer cells ⇒ measles, adenovirus, HSV-1, etc.
- Can be engineered to specifically target and replicate in cancer, express therapeutic transgenes

95
Q

how does viral lysis work in oncolytic viral therapy?

A

Viral lysis kills cells and releases viral progeny and tumor antigens stimulating host anti-tumor immunity ⇒ directly kills the cancer cell and then spreads the progeny of the virus
- Tumor antigens are also being released at the same time which stimulates the hosts anti-tumor immunity on a second level

96
Q

what is great about oncolytic viral therapy?

A

this therapy type can be engineered to only replicate in tumor cells with certain promoters so it does not lyse the other cells

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