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21 fall: Biochem > Test 3: 51-52 > Flashcards

Test 3: 51-52 Flashcards

1
Q

what are some variables that make a person susceptible to cancers

A

gender and ethnicity, health status, nutrition, young age and genetics

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2
Q

Chemically induced and ___ induced mutations are thought to be causative factor in a large majority of human and animal cancers.

A

oxidative stress

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3
Q

Most cancers are “___” in origin

A

clonal

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4
Q

what does it mean when cancer is clonal in nature

A

cancer begins with genetic and metabolic changes in one or a few cells. These cells then duplicate/ clone rapidly and lead to malignant cells

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5
Q

vogelstein model

A

how cancer forms:

Mutations in the tumor suppressor genes APC and DCC drive the progression of colon epithelial cancer. K-Ras mutation augments proliferation of cells carrying mutations further increase the chances of accumulating additional mutations. P53 is another important tumor suppressor gene and its mutation culminates in the formation of full blown carcinomas, and metastasizing tumors

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6
Q

steps of chemical carcinogenesis

A

chemical carcinogens get taking into the body and activated by cytochrome P450 to become activated carcinogens (UCs).

they body tries to stop by carcinogen inhibitors but mutations in Class II drug metoblizing enzymes leads to UCs binding to DNA and causing mutations

tumor promoters cause cell division of bad cells into hyperplastic nodules

tries to block with cis Retinols, diallyl sulfide and perillyl alochol but if unsuccesful will become neoplasia (cancer)

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7
Q

Cancer is a multi-step process and involves a series of mutational events, changes in metabolic profiles, cell cycle ___, and large scale changes in gene ___pattern.

A

regulation

expression

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8
Q

Simple steps involved in chemically induced cancer:

A

Tumor initiation (mutations induced by DNA reactive chemicals)

tumor promotion (changes in cell cycle progression rapid cell division and changes in gene expression) leading to the formation of hyperplastic nodules

progression to full blown cancer

metastasis.

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9
Q

Most chemical carcinogens are inert and they need to be ___ by the host enzyme system.

A

activated

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10
Q

Chemicals activated by ___ enzyme systems contain reactive groups (chemical radicals), or electron deficient group. A majority of them are detoxified by the class II drug metabolizing systems.

A

cytochrome P450

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11
Q

Binding of activated chemicals to DNA and induction of mutations in the critical genes is regarded as the ___step

A

initiation

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12
Q

Tumor promotion is essentially amplification of cells carrying mutations by agents that induce ___ and ___

A

cell cycle progression and cell proliferation

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13
Q

in ___ stage the tumor is still benign and may grow into nodules. At this stage they can be treated surgically, X-ray irradiation or by chemotherapeutic agents

A

hyperplastic

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14
Q

last step of cancer, tumors are aggressive, resistant to apoptosis, ___into other tissues, and cause tissue or system failure. They can still be treated surgically or by new generation of drugs that target specific molecules or signaling pathways that are either specific or predominate in tumor cells.

A

metastasize

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15
Q

tumor initiators

A

broadly classified as chemical carcinogens. They are invariably lipophilic and inert until metabolically activated by cytochrome p450 monooxygenases (class I drug metabolizing enzymes). Activated chemicals physically bind to DNA and induce mutations or chromosomal damage

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16
Q

tumor initiators are invariably ___ and inert until metabolically activated by ___

A

lipophilic

cytochrome p450 mono-oxygenases (class I drug metabolizing enzymes).

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17
Q

tumor promotors

A

chemicals, which induce cell proliferation and amplify the mutational damage or help populate the damaged cells. These compounds do not directly bind to or interact with DNA and are not mutagenic. Their action is mostly epigenetic in nature

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18
Q

___ are chemicals, which induce cell proliferation and amplify the mutational damage or help populate the damaged cells.

A

tumor promoters

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19
Q

Tumor promoters do not directly bind to or interact with DNA and are not ___ . Their action is mostly ___ in nature

A

mutagenic

epigenetic

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20
Q

tumor inhibitors

A

A) chemicals which detoxify activated carcinogens by direct binding or by altering the electrophylic property of carcinogens. Examples are GSH and gulcuronic acid and their specific transferases enzymes (class II drug metabolizing enzymes)

Chemicals which cause tumor regression by altering the transcription activity of genes involved in cell cycle regulation and cell proliferation

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21
Q

examples of tumor inhibitors are

A

GSH and gulcuronic acid and their specific transferases enzymes (class II drug metabolizing enzymes)

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22
Q

___ are chemicals which detoxify activated carcinogens by direct binding or by altering the electrophylic property of carcinogens.

A

tumor inhibitors

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23
Q

tumor inhibitors cause tumor regression by altering the ___ of genes involved in cell cycle regulation and cell proliferation

A

transcription activity

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24
Q

Cytochrome P450 (___ metabolism) enzymes play direct roles in the metabolic activation of carcinogens:

A

class I drug

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25
Q

Metabolic activation of carcinogens to reactive (electron deficient) forms requires a specific CYP isoenzyme, ___ as an electron donor, and ___ as the source of electrons

A

cytochrome P450 reductase

NADPH

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26
Q

In the reaction cycle, CYP gets reduced by the transfer of a pair of electrons from ___ and reduced CYP binds to the substrate and O2 and catalyzes the ___ of substrate.

A

CYP reductase,

oxidation

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27
Q

mechanism of tumor initiation by metabolically activated by a fungal product often contaminates food and feed, ____

A

aflatoxin B1

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28
Q

Although majority of chemical carcinogens require activation by the CYP monooxygenase system, please note that an important group of environmental/industrial pollutants belonging to the family of ___, are not metabolized by any of the known class I or class II enzymes

A

polychlorinated biphenyls (PCB)

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29
Q

___ belongs to a large family of polycyclic aromatic hydrocarbons that are found in auto exhaust, industrial combustion, cigarette smoke, byproducts of oil and coal industry.

A

Benzo(α)pyrene (BaP)

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30
Q

BaP are potent tumor ___

A

initiators

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31
Q

Activation of Bap requires ___ that are abundantly found in the hepatic and lung ER fraction (widely called as microsomes) and ___ that is also present in the microsomal fraction of most tissues

A

CYP1A1 (or 1B1)

CYP reductase

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32
Q

The activation of BaP occurs by forming ___ in place of a double bond

A

epoxides

33
Q

Epoxides only on certain position of BaP are reactive to ___ residues on DNA

A

purine

34
Q

Often epoxides are converted to ___ by the action of epoxide hyrolase.

A

diols

35
Q

Since BaP contains many double bonds, it can bind to CYP several times and undergo ___ at different position

A

epoxidation

36
Q

Only the ___ epoxide of BaP is highly DNA reactive.

A

9:10

this formation will bind easily to the N-7 of guanine of DNA

37
Q

Most mammalian, avian and aquatic species are sensitive to ___ B1 induced liver damage and hepatic cancer.

A

aflatoxin

38
Q

The aflatoxin B1 epoxide is detoxified by conjugation to ___.

A

GSH

39
Q

where is aflatoxin B1 found

A

fungal toxin, can be found on contaminated peanuts, grains, beans and animal feeds

mold = aspergillus flavis

40
Q

___ are agents that induce cell cycle and cell proliferation.

A

Tumor Promoters

41
Q

some examples of tumor promoters

A

phenobarbital and other barbiturates, alcohol, asbestos, cigarette smoke, lipopolysaccharide and other cytokines, phorbol myristate acetate, plant alkaloids, some food additives, and others

42
Q

. Proliferation of cells carrying mutations in the critical genes associated with oncogenic transformation results in accumulation of population of cells that have ___ regulatory controls

A

escaped

43
Q

proliferating mutated cells produce increased ___ because of altered metabolism and accumulate more mutations and become highly ___ even in the absence of any external stimuli.

A

ROS

proliferative

44
Q

tumor promotors act like a ___ on cells that have already acquired one or more carcinogenic mutation, causing them to divide and go through ___, increasing the likelihood that they will acquire more mutations

A

growth factor

S-Phase

45
Q

___ represent a Large Family of Non-biodegradable Industrial Pollutants and Carcinogens

A

PCBs

46
Q

___ are a group of 209 aromatic chemicals formed by the chlorination of biphenyls that were widely used as pesticides, defoliating agents, and in various industrial setting until 1979

A

Polychlorinated biphenyls PCBs

47
Q

___ are highly resistant to heat, fire, acids, and they are also non-biodegradable

A

PCBs

PCB, TCDD, DDT, Arochlor, Phenochlor and various organopesticides including “agent orange”

48
Q

Unlike other families of carcinogenic compounds listed such as benzo(a)pyrene and aflatoxin B1 above, PCBs are not metabolized by the ___ and once ingested, they remain in the body until ___

A

CYP enzymes

death

49
Q

PCBs are associated with many pathological conditions including ___, tissue inflammation and cancer.

A

oxidative stress

50
Q

Due to the high lipid solubility and slow metabolism rate of these chemicals, PCBs accumulate in the ___tissues of almost all organisms

A

fat rich

51
Q

PCBs cause:

A
  • Probable human carcinogen (breast, bone, brain and skin cancer)
  • Endocrine disrupter (binds to estrogen and thyroid hormone receptor and activates aryl hydrocarbon receptor)
  • Reproductive toxicity (induces oxidative stress and protein kinase C cascade)
  • Neurotoxicity
  • Immune system suppression
52
Q

PCBs binds to estrogen and thyroid hormone receptor and activates ___ receptor

A

aryl hydrocarbon

53
Q

PCBs cause reproductive toxicity by induces oxidative stress and ___ cascade

A

protein kinase C

54
Q

hyper active P450 1 A1 and hypo active NAT are common gene mutations in what ethnicity?

A

african americans

55
Q

hyper active P4501A1, inactive GSTM1 and slow active epoxide hydrolase are common gene mutations in what ethnicity?

A

american whites

56
Q

hyper active P4501A1 and slow glycyronyl transferase are common gene mutations in what ethnicity?

A

hispanic and asians

57
Q

___ are chemicals which detoxify activated carcinogens

A

carcinogen inhibitors

58
Q

examples of carcinogenic inhibitors

A

antioxidants

butylated hydoxy anisole

aromatic isothiocyanates

flavones

59
Q

antioxidants such as __ and __ will neutralize electron __ groups

A

Vitamin C and Vitamin E

deficient

60
Q

butylated hydorxy anisole will induce ___ like glutathione S transferase and glucuronide transferase

A

class II drug metabolizing enzymes

61
Q

___ come from cruciferous vegtables

A

aromatic isothiocyantes

62
Q

isthiocyanates induce __ enzymes.

A

class II drug metabolizing

(phenethyl isothiocyanates is an inhibitor to lung cancer)

63
Q

___ found in fruit and vegetables induce class II drug metabolizing enzymes

A

flavones

64
Q

one gene targeted by perilly alcohol is ___

A

IGF BP3 (insulin like growth factor binding protein 3)

which is an extercellular secreted protein

65
Q

Many tumor cells over express ___ growth factor. Increased extracellular level of ___ essentially blocks the growth factor inducing apoptosis in tumor cells

A

IGF1

IGF-BP3

66
Q

Compound MF-tricyclic selectively inhibits ___, the inducible form of enzyme involved in prostanoid biosynthesis.

A

cycloxygenase2 (COX2)

67
Q

___ is an important early indicator of tumor development.

A

COX2

68
Q

Compound L353381 is selective estrogen modulator (SEM) that inhibits ___ activity in breast cancer cells without affecting estrogenic activities of bone, brain and cardiovascular system.

A

estrogen receptor

69
Q

L353381 compound has several advantages over currently used drug Tamoxifen for treatment of breast cancer since it does not induce ___cancers usually associated with Tamoxifen

A

ovarian or endometrial

70
Q

Compound LG100268 is a ligand that activates some of the “orphan” retinoic acid receptors called ___, thus helps activation of several of the genes whose expression is lost or subdued in various cancers of epithelial cell origin (lung, breast, intestinal etc.).

A

RXR

71
Q

By recruiting or activating ___, LGF100268 helps restore the transcription of important genes (probably some tumor suppressor genes and genes involved in cell cycle control) by activating an otherwise silent transcription factor.

A

RXR

Most of these cancers typically show the loss (deletion) of an important transcription factor, RARβ.

72
Q

___ is used to prevent intestinal cancers

A

MF- tricyclic

73
Q

___ and ___ are used to prevent breast cancer

A

L353381

LG100268

74
Q

___: an isoflavole (3,5,4’ trihydroxy-trans-stilbene) from the roots of Japanese Knotweed, used in herbal medicine in eastern part of Asia is a potent “Aryl Hydrocarbon Receptor, Ahr” antagonist.

A

Resveratrol

75
Q

By inhibiting the activation of ___, and thus restricting the expression of CYP 1 family genes, Resveratrol protects against cigarette and environmental toxins induced lung, intestinal and breast cancer.

A

Aryl Hydrocarbon Receptor,

76
Q

___: A polyisoprenylated benzophenone and its derivative isogarcinol from Garcinia Indica fruit have potent anticancer activities on multiple tissue cancers.

A

garcinol

77
Q

Recent studies show that garcinol are potent inhibitors of ___ and other ___ proteins. The anticancer effects of these compounds are directly related to inhibition of histone modification and chromatin remodeling.

A

p300

HAT (histone acetyltransferase)

78
Q

how does BaP become carcinogentic

A

cytochrome P4501A1 and 1B1 out on reactive epoxide groups on BaP

epoxide hydrolase breaks them down to less toxic form but this causes more problems and creates 9,10 which binds easily to DNA and causes mutations

21 fall: Biochem (44 decks)

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