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BHP Exam 2 > Neoplasia II > Flashcards

Neoplasia II Flashcards

1
Q

What do cyclins do?

A
  • start cells into proliferation

- cell going through its cycle is controlled by synthesis, degradation, and state of phosphorylation of these proteins

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2
Q

Cyclins form complexes with what two things to modulate cell division?

A
  1. cyclin-dependent kinases (CDKs)

2. cyclin-dependent kinase inhibitors (CDKIs)

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3
Q

Cell cycle

A 
G1 interphase/G1-S transition
S interphase
G2 interphase
G2-M transition
M mitosis
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4
Q

Why are there checkpoints in the cell cycle?

A

designed to stop damaged cells from replicating

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5
Q

The G1 interphase/G1-S transition can only occur when what transcription factor is free in the nucleus?

A

E2F (regulated by Rb phosphorylation)

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6
Q

What occurs during S interphase?

A

cells replicate DNA

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7
Q

What regulates G2-M transition?

A

CDK1-cyclin B complex

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8
Q

What are interphase cells?

A

those in phases G1, S, and G2 (non-mitosis)

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9
Q

Following Mitosis, phase cells can which two ways?

A

non-dividing state (G0) or continue to the cell cycle

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10
Q

checkpoints

A

G1/S restriction point (R) regulated by the state of phosphorylation of Rb
-on phosphorylation of Rb, the E2F transcription factor is liberated allowing progression into S phase

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11
Q

What does the intra S checkpoint monitor?

A

errors in transcription forks

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12
Q

What does the G2/M checkpoint monitor?

A

assembly of the mitotic spindle apparatus

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13
Q

If replication errors cannot be corrected by the checkpoints, what happens?

A

apoptosis or DNA repair mechanisms

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14
Q

DNA damage

A

abnormal or absent P53

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15
Q

Why is the expression of P53 gene to make p53 protein important?

A

it increases cyclin dependent kinase inhibitor (CDKI) p21 protein (WAF1) which prevents phosphorylation and arrests cell cycle

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16
Q

What happens when there’s an abnormal or absent p53?

A

regulatory function impaired

or cells with damaged DNA complete mitosis and thus propagate a mutation

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17
Q

Where do neoplastic transformations come from?

A

abnormalities in genes that regulate cell proliferation

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18
Q

What are the 4 main genetic mechanisms of neoplastic transformation?

A
  1. oncogenes
  2. tumor supressor genes (anti oncogenes)
  3. anti-apoptotic genes
  4. loss of cellular repair gene products
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19
Q

What kind of gene is the p53?

A

tumor supressor gene

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20
Q

What do oncogenes cause proliferation of?

A

Abnormal mitotic cells that should not be there

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21
Q

What do anti-apoptotic genes do?

A

keep cell from being killed

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22
Q

oncogenes

A
  • derived by mutations
  • expressed dominantly
  • promote growth in absence of normal growth promoting signals
  • their products, oncoproteins, are devoid of normal regulatory elements
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23
Q

Where are abnormalities of oncogenes found?

A

tumors (primary events in malignant transformation)

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24
Q

What do oncogenes do?

A
  • don’t respond to normal growth factors
  • increase secretion of growth factor independently of what the body needs
  • increase the number of receptors
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25
Q

What are the three kinds of oncogenes originally isolated from tumor forming RNA retroviruses?

A
  • V-oncs (viral oncogenes)
  • C-oncs (Cellular oncogenes)
  • P-oncs (proto-oncogenes)
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26
Q

V-oncs (Viral oncogenes)

A

genes within a virus that code for a protein involved in the development of neoplasia

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27
Q

C-oncs (cellular oncogenes)

A

genes that code for proteins in the development of neoplasia

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28
Q

P-oncs (proto-oncogenes)

A

genes that code for proteins involved in control of cell growth

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29
Q

two point mutation examples

A

Rb and P53

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30
Q

tumor supressor genes (anti-oncogenes)

A
  • loss of activity of genes which produce products that inhibit cell growth
  • generally act in a recessive manner to produce tumors
  • malignant phenotype only develops if both alleles of a gene fail to suppress growth
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31
Q

What does the absence of tumor supressor genes promote?

A

neoplasia!

- tumor suppressor genes are gatekeepers that normally direct control cellular growth (Rb, P53, APC)

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32
Q

Rb

A
  • first tumor suppressor gene discovered
  • on chromosome #13
  • found in many other tumors
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33
Q

What is the most common genetic abnormality ?

A

p53**

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34
Q

APC

A

Adenomatous polyposis coli

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35
Q

What are the 2 forms of Rb?

A

familial and sporadic

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36
Q

familial form of Rb

A
  • affected children have one mutant gene(inactive) and one normal gene (active)
  • if the second gene undergoes somatic mutation, tumor will develop (both gene alleles must undergo mutation)
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37
Q

When is P53 activated?

A
  • in response to DNA damage–> cell cycle arrest and DNA repair
  • if repair not achieved, p53 causes cell to enter apoptotic pathway of cell death
  • loss of p53 activity allows proliferation of cells with DNA damage
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38
Q

APC (adenomatous polyposis coli) progression

A
  • inherit a single inactive copy=> multiple benign adenomata of the large bowel
  • if cells develop a second mutation of the normal inherited gene on the other allele–> carcinoma of the colon
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39
Q

anti-apoptotic genes

A
  • overexpression of genes for anti-apoptosis protein (bcl-2)

- prevents normal cell death (failure to eliminate genetically damaged cells)**

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40
Q

What does the loss of DNA repair systems activity lead to?

A
  1. DNA instability

2. somatic mutations in oncogenes or tumor supressor genes

41
Q

DNA repair genes

A

-well developed system of detection and repair of DNA (sometimes called “caretaker” genes)

42
Q

philadelphia chromosome

A

translocation between chromosomes 9 and 22; found in leukemia

43
Q

What are the 4 chemical carcinogens in Neoplasia?

A
  1. polycyclic hydrocarbons
  2. aromatic amines
  3. nitrosamines
  4. aklyating agents
44
Q

polycyclic hydrocarbons

A
  • tar; potent agents in cigarette smoke

- cause lung cancer

45
Q

aromatic amines

A
  • industrial exposure (rubber, dye) and converted to active agents in the liver; concentrated in the urine
  • primarily bladder cancer
46
Q

nitrosamines

A
  • bacteria in gut converts dietary nitrites and nitrates to nitrosamines
  • GI tract tumors
47
Q

alkylating agents

A
  • bind directly to DNA and are directly mutagenic

- used in cancer chemotherapy (e.g.. cyclophosphamide)

48
Q

What are the 3 stages of chemical carcinogenesis?

A
  1. initiation
  2. promotion
  3. progression
49
Q

inititation (carcinogenesis)

A

-induction of genetic changes in cells (altered genome)

50
Q

promotion (carcinogenesis)

A
  • induction of cell proliferation via mitogenic or cytotoxic mechanism
  • initially reversible if promoting agent is withdrawn
51
Q

progression

A
  • persistent cell proliferation–>
  • initiated cells acquire secondary genetic abnormalities in oncogenes–> dysregulation
  • autonomous cell growth–> invasive neoplasm with subclones
52
Q

key facts: chemical carcinogens

A

-most info from animal studies
-following exposure there is a LONG LATENT PERIOD before neoplasm develops
(-altered cells are primed but require second change to bring about molecular genetic changes expressed as neoplasia)

53
Q

What are 2 main effects of DNA damage through irradiation (neoplasia)

A

DNA breaks and instability

54
Q

direct exposure (e.g. x-rays) increases risk of tumors in bone marrow and skin of exposed areas

A
  • environmental exposure more complex issue
  • radon increases risk of carcinoma of the lung
  • radioactive iodine therapy increases risk of thyroid carcinoma
  • incorporation of radioactive metals into bone increases the risk of tumors of bone marrow and bone
55
Q

ultraviolet light

A

major cause of neoplasia esp. many types of malignant skin tumors

56
Q

what is the physical agent of asbestos induced neoplasia?

A

inhaled asbestos fibers

57
Q

Preneoplastic conditions

A

-increased risk of neoplasia

hyperplasia, dysplasia, and chronic immune diseases

58
Q

hyperplasia in preneoplastic conditions

A
  • endometrial

- epithelial hyperplasia of breast lobules and ducts

59
Q

dysplasia in preneoplastic conditions

A
  • chronic gastritis predisposes CA of stomach
  • chronic colitis predisposes CA of the colon
  • hepatic cirrhosis predisposes liver cell CA
60
Q

chronic immune diseases in preneoplastic conditions

A
  • celiac disease predisposes gut lymphoma

- autoimmune thyroiditis predisposes thyroid lymphoma

61
Q

immune response in neoplastic disease

A

tumors display abnormal antigens

  • an immune response against tumor may occur
  • weak
  • not effective in eradicating an established tumor
62
Q

CA

A

carcinoma

63
Q

oncofetal antigens

A
  • normally expressed only during development

- become re-expressed in the less differentiated neoplastic cells

64
Q

incidence of lung cancer is increasing rapidly in women as a result of

A

cigarette smoking (>deaths than breast cancer)

65
Q

Cancer facts

A
  • survival rate for many tumors has greatly increased over past 25 years with advancement in treatment
  • cancer prevention strategies depend on elimination of causative factors
  • cancer detection strategies depend on screening population for early forms of neoplasia at an early stage of development
66
Q

tumor markers

A

tumors liberate products that can be detected in blood samples

  • may aid diagnosis
  • also use to follow up therapy
  • -> blood levels become increased if tumor recurs
  • -> often before imaging can detect
67
Q

tumor marker: AFP= alpha Fetoprotein

A

hepatocellular carcinoma and

germ cell tumors

68
Q

tumor marker: human chorionic gonadotropin (hCG)

A

trophoblastic tumors

69
Q

tumor marker: Acid phosphasase

A

prostatic carcinoma

70
Q

tumor marker CEA =Carcinoembryonic antigen

A

Gastrointestinal tract neoplasia

71
Q

tumor marker hormone products

A

endocrine tumors

72
Q

novel anti-cancer drugs

A

-inhibitors of specific proteins in tumor cells (proteins involved in cell cycle entry and progression) or specific second messenger pathways

73
Q

novel anti-cancer drugs

A

molecular pathology= can detect the specific target by screening patients prior to treatment

74
Q

breast cancer drug (screening targe)

A

Herceptin (trastuzumab) (HER-2)

75
Q

breast cancer mechanism of action

A
  • herceptin
  • binds to HER2, a member of the EGF-receptor family of proteins
  • binding of Herceptin reduces the activation of the HER2-linked tyrosine kinase
  • induces activation of the cell cycle inhibitors p21 and p27
76
Q

What is the gastrointestinal stromal tumors (GIST) target?

A

Glivec

77
Q

gastrointestinal stromal tumors (GIST)

A

Glivec is an inhibitor of the receptor tyrosine kinases for PDGF and stem cell factor (SCF) c-kit

  • inhibits PDGF and SCF mediated cellular events
  • in vitro inhibits proliferation and induces apoptosis in GIST cells, which express and activating c-kit mutation
78
Q

tumor supressor genes

A

anti-oncogenes

79
Q

What chromosome is p53 on?

A

chromosome 17p13

80
Q

What does APC degrade?

A

degrades alpha catenin so if defective then alpha catenin levels rise in the cell and drive cell proliferation

81
Q

What do mutations in DNA repair allow?

A

proliferation of cells with DNA mutations, replication error positive (RER+) phenotype

82
Q

What leads to tumor heterogeneity?

A

tumors accumulate mutations

83
Q

What is tumor heterogeneity?

A

multiple oncogene abnormalities in a single tumor

84
Q

What is a complete carcinogen?

A

environmental agent that is both an initiator and promotor

85
Q

*association with mesothelioma of the pleura is particularly strong

A

asbestos induced neoplasia

86
Q

What is RER+ phenotype?

A

replication error positive

87
Q

potent cause of neoplasia of lung and pleura

A

asbestos induced neoplasia

88
Q

How are DNA repair genes assessed?

A

looking at tandem repeated DNA sequences in cells which normally remain constant
–> In DNA repair errors, cells develop changes in the repeat length of microsatellite DNA –> microsatellite instability

89
Q

What is herceptin?

A

monoclonal antibody relating to breast cancer

90
Q

2 types of antigens in immune response of neoplastic disease

A
  1. tumor specific antigens

2. tumor associated antigens

91
Q

What is the 2nd most common cause of death in developed countries

A

cancer

92
Q

What is the 1st most common cause of death in most developed countries (23% of all mortalities)

A

ischemic heart disease

93
Q

What causes incidence of different histological types of cancer to vary greatly b/w different populations?

A

occupational, social, and geographic factors

94
Q

What cancer is increasing among caucasians in many countries?

A

malignant melanoma of the skin

95
Q

What is a multistage process involving initiation, promotion, and progression?

A

Carcinogenesis

96
Q

Where is there a high incidence of stomach cancer compared to other countries (smoked raw fish)?

A

Japan

97
Q

How does tumor heterogeneity occur?

A
  • endothelial cells in capillary release protein growth factors
  • malignant cells release angiogenic proteins and supress levels of angiogenesis inhibitors
98
Q

What are genes that promote autonomous growth in cancer cells?

A

oncogenes

99
Q

What are two examples of oncofetal antigens?

A
  1. alpha fetoprotein (AFP) (hepatocellular carcinoma)

2. carcinoembryonic antigen (CEA) (Gastrointestinal tract malignancies)

BHP Exam 2 (6 decks)

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