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Tissues > T28 - Carcinogenesis II > Flashcards

T28 - Carcinogenesis II Flashcards

1
Q

What are the three categories of physical agents that play a role in carcinogenesis?

A

chemical carcinogens

radiant energy

microbial agents

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2
Q

What is immune surveillance?

A

immune system’s surveilling the body for premalignant and malignant cells

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3
Q

What are the two subdivisions of chemical carcinogens?

A

direct-acting agents

indirect-acting agents

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4
Q

Describe the difference between direct-acting and indirect-acting agents in chemical carcinogens.

A

direct-acting agents require no prior metabolic conversion = weak carcinogens

indirect-acting agents erquire metabolic conversion (e.g. hydrocarbons in fossil fuels or benzo-a-pyrene in cigarette smoke)

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5
Q

What is the relationship between indirect chemical agents and cancer susceptibility?

A

because indirect agents require metabolic activation, enzymatic pathways involved in activation can impact cancer susceptibility (e.g. everyone inherits different cytP450 enzymes, so different susceptibilities to cancer)

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6
Q

What is aflatoxin B1?

A

DNA mutagen produced by strains of Aspergillus flavus in improperly stored grains and nuts (i.e. peanuts)

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7
Q

Aflatoxin B1 causes

A

hepatocellular carcinoma

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8
Q

How is carcinogenicity commonly tested?

A

expose a rodent to the carcinogen and then monitor for tumor onset and growth

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9
Q

What is the mechanism of action for chemical carcinogens?

A

contain highly-reactive electrophiles that bind to DNA and cause mutations

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10
Q

What are the two types of radiation carcinogens?

A

ionizing radiation

UV rays

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11
Q

Ionizing radiation has what effect on DNA?

A

causes chromosomal breakage and aberrations

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12
Q

Give a historical example of ionizing radiation that led to increased cancer prevalence.

A

Chernobyl nuclear disaster led to higher rates of thyroid cancer

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13
Q

How do UV rays affect DNA?

A

induce formation of pyrimidine dimers

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14
Q

Give an example of a tumor that results from UV ray damage of DNA.

A

melanomas (skin cancers in general)

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15
Q

What is the only retrovirus that has been definitively shown to be directly carcinogenic?

A

HTLV-1

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16
Q

HTLV-1 is endemic to (2)

A

the Caribbean

Japan

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17
Q

HTLV-1 causes

A

T-cell leukemia, because it has a tropism for CD4+ T cells

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18
Q

Explain on a cellular level how HTLV-1 causes T-cell leukemia. (4)

A

HTLV-1 genome encodes TAX viral protein → TAX activates cytokine genes and associated receptors in T cells → autocrine and paracrine loops cause T cells to proliferate → polyclonol process

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19
Q

Give an example of an oncogenic RNA virus.

A

HTLV-1

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20
Q

Give four examples of oncogenic DNA viruses.

A

Epstein-Barr virus

human papilloma virus (HPV)

hepatitis B virus (HBV)

hepatitis C virus (HCV)

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21
Q

Epstein-Barr virus has been implicated in the pathogenesis of what human tumors? (4)

A

Burkitt lymphoma

B-cell lymphomas in AIDS patients

Hodgkin lymphoma

nasopharyngeal carcinoma

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22
Q

Explain, on a cellular leve, how the Epstein-Barr virus contributes to tumor pathogenesis. (2)

A

EBV gene products stimulate B-cell proliferation

EBV binds to and infects B cells through CD21, a type 2 complement receptor

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23
Q

What is a gross consequence of HPV?

A

benign squamous papillomas (warts)

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24
Q

What are the low risk subtypes of HPV? (2)

A

HPV-6

HPV-11

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25
Q

What are the high risk HPV subtypes? (2)

A

HPV-16

HPV-18

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26
Q

The oncogenic potential of HPV originates from what genes?

A

viral genes E6 and E7

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27
Q

Describe the roles of viral genes E6 and E7 in HPV oncogenesis.

A

E6 binds to and mediates degradation of p53

E7 binds to and mediates degradation of RB

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28
Q

What are the properties of hepatitis B virus (HBV)? (3)

A

does not directly make the cancer-causing genes (unlike HTLV)

associated with liver cancer due to inflammation

continued proliferation caused by HBV causes DNA damage and gene mutations that are oncogenic

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29
Q

What is the transcription factor associated with HBV?

A

HBV encodes transcription factor HBx, which can activate TGFb1 and IGF1 growth factors and inhibit p53

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30
Q

(T/F) HCV is a DNA virus.

A

False. Hepatitis C virus is not a DNA virus (it’s an RNA virus), but like HBV is strongly linked to liver cancer.

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31
Q

What are heliobacter pylori and where are they found?

A

gram-negative bacteria that reside between mucus layer of stomach and gastric epithelium

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32
Q

Why is heliobacter pylori unique in the context of carcinogenesis?

A

first bacterial organism to be classified as a carcinogen

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33
Q

H. pylori is responsible for causing what two tumors?

A

gastric adenocarcinoma

gastric lymphoma

34
Q

What are the clinical symptoms of gastric adenocarcinoma caused by H. pylori?

A

chronic inflammation of gastric epithelium (i.e. chronic gastritis)

35
Q

H. pylori-related lymphomas have what cellular origin?

A

B-cell origin

36
Q

The B-cells implicated in H. pylori-induced gastric lymphoma reside where?

A

reside in marginal zones of gastric lymphoid follicles → hence the name MALT lymphomas

37
Q

How does the H. pylori-induced infection of B cells lead to neoplastic transformation?

A

chronic inflammation and stimulation of marginal zone B cells leads to DNA damage and neoplastic transformation

38
Q

How is MALT lymphoma treated?

A

assuming early detection, can be treated with antibiotics to cure H. pylori infection

39
Q

Differentiate between tumor specific and tumor associated antigens.

A

tumor specific antigens are only found on tumor cells

tumor associated antigens are found on tumor cells and on some normal cells

40
Q

What are oncofetal antigens?

A

antigens expressed during embryogenesis but disappear and are not normally expressed in adult tissues

41
Q

Give two examples of oncofetal antigens.

A

carcinoembryonic antigen (CEA)

alpha-fetoprotein (AFP)

42
Q

What is carcinoembryonic antigen?

A

luminal glycoprotein involved in cell adhesion

43
Q

Carcinoembryonic antigen is associated with what malignancies? (2)

A

inflammatory and cancerous lesions of both the colon and pancreas

44
Q

What is the clinical utility of the carcinoembryonic antigen?

A

because of its lack of specificity for cancer, it’s most useful for monitoring recurrence of carcinomas after surgery

45
Q

What is alpha-fetoprotein?

A

glycoprotein globulin secreted by fetal liver and yolk sac

46
Q

Alpha-fetoprotein is associated with what malignancies?

A

alpha-fetoprotein is expressed by:

hepatocellular carcinomas

testicular cancers/teratomas (i.e. germ cell tumors)

yolk sac tumors (i.e. endodermal sinus tumors)

47
Q

Give two examples of glycoproteins (apart from oncofetal antigens) that can serve as tumor antigens.

A

gangliosides

mucins

48
Q

Describe how gangliosides can serve as tumor antigens.

A

normal in composition, but overexpressed in melanomas and colon cancers

49
Q

Describe how mucins can serve as tumor antigens.

A

under-glycosylated

50
Q

As tumor antigens, mucin are associated with what malignancies? (4)

A

carcinomas:

breast

pancreatic

ovarian

colon

51
Q

Differentiate between mucin CA-125 and mucin CA-19-9.

A

CA-125: blood marker expressed in ovarian cancers, but NOT specific

CA-19-9: blood marker sensitive but NOT specific to pancreatic cancer

52
Q

How does Gleevec/Imatinib cure/treat CML?

A

it poisons the BCR-ABL fusion protein

53
Q

Give three examples of oncogenes that, when mutated, produce peptides only found in tumor cells.

A

p53

RAS

CDK4

54
Q

Give two examples of non-mutated proteins that can be overexpressed, conferring tumor immunity.

A

HER2/NEU (in breast cancer)

tyrosinase (in melanomas)

55
Q

What is Herceptin?

A

anti-HER2/NEU antibody

56
Q

What is the predominant anti-tumor mechanism?

A

cell-mediated immunity

57
Q

What are the four classes of anti-tumor immune effector mechanisms?

A

cytotoxic T cells

natural killer (NK) cells

macrophages

humoral mechanisms

58
Q

What is the role of cytotoxic T cells in antitumor effector mechanisms? (2)

A

protects against virus-associated neoplasms

requires prior exposure (i.e. immunization)

59
Q

What is the role of natural killer cells in antitumor effector mechanisms? (3)

A

kill without prior sensitization (in contrast to cytotoxic T cells)

activated by IL-2

active against tumor cells with low MHC Class I expression

60
Q

What is the role of macrophages in antitumor effector mechanisms? (2)

A

produce reactive oxygen species or TNF to kill tumor cells

61
Q

What is the role of humoral mechanisms (antibodies) in antitumor therapy?

A

monoclonal antibodies against tumor markers used in therapy (i.e. anti-CD20)

62
Q

Carcinogenesis obviously occurs in patients without immune deficiencies. What are three mechanisms by which tumors evade the host immune system?

A

selective outgrowth of antigens (disguise)

lost/reduced expression of histocompatibility molecules (hide)

spontaneous/pathogen/drug-induced immunosuppression of host (suppress)

63
Q

What are the local effects of tumors on hosts? (3)

A

destruction of normal tissues

ulceration through natural boundaries, causing hemorrhage or infection

tumor rupture or infarction

64
Q

Describe the hormonal effect of tumors on hosts. Give an example.

A

over-production of hormones native to tumor origin

for example:

insulinoma of pancreas

65
Q

What is cancer cachexia?

A

progressive loss of fat + muscle leading to wasting, weakness, and anemia

66
Q

What causes cancer cachexia?

A

caused by excess of cytokines, not just tumor metabolism

67
Q

Define paraneoplastic syndrome.

A

symptoms not accounted for by local or distant spread of tumor

68
Q

Give three examples of paraneoplastic syndromes.

A

endocrinopathies (lung tumor making ACTH)

neuromyopathies (lung tumor causing myasthenia gravis)

vascular/hematologic derangements (pancreatic carcinoma causing deep vein thrombosis)

69
Q

What are four tools used in the diagnosis of cancer?

A

pathology

tumor markers

molecular cancer diagnostics

molecular profiling

70
Q

What are the four substeps within pathology as a tool for the diagnosis of cancer?

A

histology

cytology

immunochemistry

flow cytometry

71
Q

What is histology, in the context of diagnosing cancer?

A

microscopic examination of formalin-fixed tissue using H&E staining

72
Q

What is cytology, in the context of diagnosing cancer?

A

microscopic examination of individual cells smeared on slide

73
Q

What are the two types of cytologic specimens?

A

exfoliative = removal of cells from tissue/organ

fine needle aspiration = use a needle + syringe to suck out cells

74
Q

What are two disadvantages of cytology?

A

limited specimen sample

no info about tissue architecture

75
Q

What is the utility of tumor markers in diagnosing cancer?

A

can be used to screen for malignancies or monitor for cancer relapse

76
Q

In what context is “minimal residual disease” detected?

A

PCR is used to detect presence of BCR-ABL transcripts in blood to monitor Philadelphia chromosome-positive CML

77
Q

Describe how molecular profiling of tumor works. (4)

A

mRNA extracted from 2 tissue sources (normal + tumor) → complementary DNA samples made → cDNA hybridized to cDNA probes in a matrix → laser detects fluorescence from each spot, allowing comparison of genome between normal + tumor

78
Q

Give three examples of techniques (and an associated malignancy) used in molecular cancer diagnostics.

A

flow cytometry = hematopoietic malignancies

FISH = CML

PCR = CML

79
Q

How does Epstein-Barr virus cause Burkett lymphoma? (4)

A

EBV stimulates B-cell proliferation → secondary mutations accumulate → t(8;14) chromosomal translocation → constitutive expression of Myc gene fused to immunoglobulin heavy chain gene

80
Q

(T/F) In HPV, E6 and E7 are sufficient to induce transformation.

A

False. RAS and other genes would be required to induce transformation — E6 or E7 on their own are not sufficient.

81
Q

What is hepatitis C virus’ mode of action? (2)

A

induction of cirrhosis and parenchymal regeneration

Tissues (23 decks)

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