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Biochemistry (Cole) > Lecture 39 Anticancer therapies radiation and drugs for cancer > Flashcards

Lecture 39 Anticancer therapies radiation and drugs for cancer Flashcards

1
Q

What are the key properties of a cancer cell?

A
  • they reproduce without regard to normal restraints on cell growth and cell division
  • they invade and colonize areas normally reserved for other cells
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2
Q

Do all cancer cells metastasize?

A
  • no
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3
Q

When are tumors considered benign?

A
  • if the neoplastic cells do not become invasive
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4
Q

When are tumors considered malignant?

A
  • if it acquires ability to invade surrounding tissue
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5
Q

What is a consequence of malignant tumors invasiveness?

A
  • they produce cells that break out of their primary site and form secondary tumors at other sites
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6
Q

What are the sites where secondary tumors are formed?

A
  • metastases
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7
Q

Is a single mutation enough to cause cancer?

A
  • no
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8
Q

What are potential risk factors for cancer?

A
  • radiation exposure
  • UV light from the sun
  • chemicals (carcinogens)
  • life-style (smoking, certain diets)
  • Viruses (EBV, HIV, HPV)
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9
Q

Where are the most common cancers of epithelia?

A
  • reproductive tract
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10
Q

Why does the risk of cancer increase with age?

A
  • the longer you live the more likely you are to develop a second hit or exposed to a cancer causing environment
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11
Q

If you are exposed to 2-naphthylamine more than 5 years what happens?

A
  • onset of cancer was earlier

- and risk increases

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12
Q

Duration of exposure does what?

A
  • increases risk and influences time of onset
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13
Q

What is p53 key in?

A
  • a key mechanism in the cellular response to DNA damage
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14
Q

If DNA damage is a critical determinant of progression to next stage, what protein is involved?

A
  • p53 involved
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15
Q

What does Mdm2 lead to?

A
  • p53 being ubiquinated and degraded
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16
Q

What happens after DNA damage in cell cycle?

A
  1. DNA damage
  2. Phosphorylation
  3. Mdm2 removed
  4. P53 binds to p21 (Cdk inhibitor)
  5. Cdk inhibitor translated and shuts down G1/s-cdk and S-cdk
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17
Q

What is p21?

A
  • a cdk inhibitor that is translated once p53 binds to its transcription factors
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18
Q

What happens is p53 doesnt function properly?

A
  • wont have brake that happens when there is DNA damage
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19
Q

What is p53?

A
  • tumor suppressor
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20
Q

What is the basic strategy for cancer treatment drugs?

A
  • to induce so much damage to tumor cells via DNA damage that they cant divide
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21
Q

What are the side effects of cancer treatment drugs?

A
  • they can have the same effects on non cancer cells
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22
Q

What is external beam therapy?

A
  • uses a machine to send high energy beams from outside the body to the tumor area
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23
Q

What is internal radiation therapy?

A
  • radioisotope given internally, radiation generally only travels a short distance depending upon the isotope and its energy
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24
Q

What treats thyroid tumors?

A
  • iodine therapy

internal radiation therapy

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25
Q

How does photon therapy work?

A
  • works either by direct ionization of atoms in the DNA chain or indirectly by ionization of water to form hydroxyl radicals that can then damage DNA
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26
Q

What does charge particle or proton therapy do?

A
  • uses a particle accelerator to beam high-energy particles (protons or carbon, boron or neon nuclei)
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27
Q

What is an advantage of proton therapy?

A
  • better ability to precisely localize the radiation dosage and less damage to surrounding healthy tissue
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28
Q

How does doxorubicin work?

A
  • doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis
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29
Q

What is another way doxorubicin works?

A
  • forms oxygen free radicals resulting in secondary cytotoxicity
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30
Q

What does bleomycin do?

A
  • forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single and double stranded breaks in DNA
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31
Q

How does cisplatin work?

A
  • inorganic platinum agent
  • forms highly reactive platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA
  • inducing intrastrand DNA cross links as wells as DNA protein cross links
  • these cross links result in apoptosis and cell growth inhibition
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32
Q

What is a side effect of cisplatin?

A
  • kidney toxcity
33
Q

What does methotrexate do?

A
  • inhibits the enzyme dihydofolate reductase, resulting in inhibition of purine nucleotide and thymidylate synthesis and subsequently inhibition of RNA syntheses.
34
Q

On a simpler level how does methotrexane work?

A
  • rate limits purine nucleotide synthesis

- dont have building blocks for DNA

35
Q

How does vinblastine work?

A
  • vinblastine binds to tubulin and inhibits microtubule formation
36
Q

What does no microtubule formation result in?

A
  • disruption of mitotic spindle assembly and arrest of tumor cells in the M phase of cell cycle
37
Q

What does vincristine?

A
  • interferes with mitotic spindle in S phase of cell cycle

- leaves tumor cells in metaphase

38
Q

What does prednisolone do?

A
  • it binds to and activates specific nuclear receptors resulting in an altered gene expression and inhibition of proinflammatory cytokine production
  • induces apoptosis
  • longterm use has affects on other cells like osteocytes
39
Q

Where do we get many of these cancer drugs?

A
  • plants
40
Q

What is prednisolone typically used for?

A
  • it is a synthetic glutocorticoid with anti-inflammatory properties
41
Q

How is prednisolone used as an anti-cancer drug?

A
  • it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production
  • also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates APOPTOSIS
42
Q

What is immunotherapy?

A
  • a treatment designed to induce enhance or suppress the immune response
  • designed to stimulate a persons own immune response to destroy cancer cells
43
Q

What has been shown to help shrink or slow growth of tumors such as melonoma, non-small cell lung cancer, and hodgkin lymphoma?

A
  • opdivo and kytruda
44
Q

What do opdivo and keytruda target?

A
  • PD-1 on T-cells
45
Q

What is PD-1?

A
  • is a part of an immune checkpoint checkpoint control system that keeps immune cells from attacking self
46
Q

What is leukemia?

A
  • an overgrowth of WBCs
47
Q

What is chronic myelogenous leukemia caused by?

A
  • a chromosomal translocation called the philadelphia chromosome
48
Q

What does the translocation on the philadelpia chromosome create?

A
  • a fusion gene/protein between the BCR gene and ABL gene
49
Q

what type of fusion protein is the philadelphia chromosome?

A
  • a tyroskine kinase
50
Q

What is leukemia characterized by?

A
  • increased production/growth of myeloid cells in the bone marrow that then circulate in the blood
51
Q

What is the parent drug used to treat CML?

A
  • gleevec
52
Q

What is the mechanism of Bcr-Abl gene formation?

A
  • bcr breaks at 5’ end
  • abl breaks near 5’ to 3’ end
  • translocation
  • transcription to fused Bcr/Abl mRNA
  • translation to Bcr-Abl fusion protein
53
Q

What is the first phase of treatment for leukemia?

A
  • induction therapy
54
Q

What is the goal of the induction phase?

A
  • to kill the luekemia cells in the blood and bone marrow and put leukemia into remission
55
Q

What is the second stage of luekemia treatment?

A
  • consolidation/intensification
56
Q

When does the consolidation phase begin?

A
  • once the luekemia is in remission
57
Q

What is the goal of the consolidation phase?

A
  • to kill any remaining leukemia cells that might not be active but could begin to regrow and cause a relapse
58
Q

What is the last phase of treatment?

A
  • maintenance therapy
59
Q

What is the goal of maintenance therapy?

A
  • to kill any remaining luekemia cells that may regrow and cause a relapse
60
Q

When are the cancer treatments given in lower doses?

A
  • the maintenance therapy phase
61
Q

Does acute myeloid luekemia have a spectrum?

A

yes

62
Q

What are the subtypes of AML based off of?

A
  • they are based upon the cell that the luekemia develops from and many chromosomal translocations that create fusion proteins
63
Q

What is the easiest form of AML to treat?

A
  • AML M3
64
Q

What is a dangerous side effect of AML 3?

A
  • patients can develop blood-clotting and bleeding problems
65
Q

What mutation leads to AML3?

A
  • a translocation of the retinoic acid receptor alpha gene (RARA) on Cs17 with the PML gene on Cs15
66
Q

What does PML-RARA fusion preotein do?

A
  • it has an altered function

- it binds with high affinity to sites on the DNA important for granulocyte differentiation

67
Q

What does the blocking of differentiation lead to from the PML-RARA fusion protein?

A
  • it leads to immature leukemic promyelocytes
68
Q

How does ATRA treat the PML-RARA fusion protein?

A
  • it induces the promyelocytes terminal differentiation and then these differentiated malignant cells undergo apoptosis
  • ATRA induces dissociation of NCOR and HDAC allowing for differentiation to proceed
69
Q

What does Acute Lymphoblastic Leukemia do?

A
  • bone marrow produces too many immature lymphocytes (at the expense of other blood cell types)
  • expense of ALL
70
Q

What are the risk factors of ALL?

A
  • exposure to x-rays before birth
  • exposure to radiation
  • past treatment with chemotherapy
  • certain changes in the genes
  • genetic conditions that include down sydrome, and bloom syndrome
71
Q

What are some signs and symptoms of ALL?

A
  • fever, foul smelling urine, easy bruising or bleeding, petechia, bone or joint pain, lumps in neck
72
Q

How would you diagnose a patient with ALL?

A
  • blood CBC, bone marrow analysis, cytogenetic analysis
73
Q

What is an important prognosis of ALL?

A
  • the number of WBC at diagnosis
74
Q

Can ALL spread to the CNS?

A
  • yes that is why intrathecal treatment is so important
75
Q

Where do most relapses of ALL come from?

A
  • spinal fluid
76
Q

If a child is 1-10 years old and have a WBC of less than 50,000 they are considered ____ risk?

A
  • low
77
Q

If a child is 1-10 years old and have a WBC of 50,000 or more at diagnosis are considered ______ risk?

A
  • high
78
Q

What drug treatment for water would make a child chunky and retain water?

A
  • prednisolone

Biochemistry (Cole) (25 decks)

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