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Pathology > carcinogenesis > Flashcards

carcinogenesis Flashcards

1
Q

Initial damages or mutations may be caused by

A

environmental exposure (acquired from exogenous agents e.g., viruses or environmental chemicals, or by endogenous products of cellular metabolism

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2
Q

why DNA repair is very important in determining if a mutation will develop?

A

If there is DNA repair, the damage will come back to normal and if the DNA repair mechanism is defective, there will be mutations.

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3
Q

tumor-specific mutations are often identified by:

A

DNA sequencing

Chromosomal analyses

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4
Q

4 classes of genes are the principal targets of cancer-causing mutations:

A
  1. Proto-oncogenes
  2. Tumor suppressor genes
  3. Genes that regulate apoptosis
  4. Genes involved in DNA repair
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5
Q

Transforming genes that promote autonomous cell growth and cause cancer

A

ONCOGENES

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6
Q

friendly” versions of oncogenes present in normal cells

A

Proto-oncogenes (p-onc)

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7
Q

Mechanism of oncogene activation

A
  1. mutation
  2. chromosomal translocation
  3. gene amplification
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8
Q

Mechanism of oncogene action

A 
Growth factors
Cell surface receptors
Intracellular transduction pathways
Transcription factors
Cell cycle proteins
Inhibition of apoptosis
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9
Q

Negative regulators of cell growth

• Anti-oncogenes

A

TUMOR SUPPRESSOR GENES

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10
Q

Describe a RB (retinoblastoma) protein

A

Governor of proliferation
• Regulator of cell cycle
• Inhibitor of G1/S transition during cell cycle progression

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11
Q

Function of P53

A

Acts as a transcription factor
Prevents propagation of genetically damaged cells
• Blocks cell cycle progression
• Encodes for the protein p53

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12
Q

Most frequently mutated gene in human cancers

A

P53

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13
Q

Gatekeeper of colonic neoplasia

A

APC (Adenomatous Polyposis Coli)/β-catenin

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14
Q

Function of APC (Adenomatous Polyposis Coli)/β-catenin

A

Decreases growth promoting signals

• Has a major role in controlling cell fate, adhesion, and cell polarity during embryonic development

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15
Q

Mutation in genes that regulate apoptosis result in

A

less cell death and enhanced survival of cells

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16
Q

Mutations in DNA repair genes impair the ability of

A

cell to recognize and repair nonlethal genetic damage in other genes

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17
Q

Cancer arises from nonlethal genetic damage which can be transmitted to

A

cell progeny

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18
Q

Promotes cell growth and requires the alteration of only 1 allele to create an out of control cellular growth (dominant gene

A

PROTO-ONCOGENES

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19
Q

3 KINDS OF GENES THAT ARE TARGETS FOR CARCINOGENIC TRANSFORMATION

A
  1. PROTO-ONCOGENES
  2. TUMOR SUPPRESSOR GENES
  3. GENES THAT REGULATE APOPTOSIS
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20
Q

Function of tumor suppressor genes

A

Inhibits cell growth and requires the alteration of both alleles to affect cell growth (recessive oncogenes

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21
Q

Ability of transformed cells to acquire further abnormal characteristics over time, independent of tumor size

A

TUMOR PROGRESSION

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22
Q

What are the abilitie that a tumor acquires in tumor progression

A

ability to invade
ability for metastatic spread
ability to develop anaplasia

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23
Q

Oncogenes are cancer-causing genes derived from proto-oncogenes by:

A

Mutation
Retroviral transduction
Gene amplification or dislocations

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24
Q

Oncogenic receptors exist in a

A

prolonged “on” state, even in the absence of bound growth factor

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25
Q

codes for receptors associated with glial cells

A

RET proto-oncogene

26
Q

Point mutations in the RET proto-oncogene (codes for receptors associated with glial cells) are associated with

A

multiple endocrine neoplasia (MEN) and familial medullary thyroid carcinoma

27
Q

Exist on the inner plasma membrane and following activation work to phosphorylate cytoplasmic proteins

A

Signal Transducing Proteins

28
Q

A GTP-cleaving protein receptor associated transducing protein

A

RAS

29
Q

function of MAP (mitogen activated protein

A

increases nuclear transcription factors

30
Q

Normally works to activate MAP

A

RAS

31
Q

Forms a heterodimer with MAX protein forming the MYC-MAX combination which activates transcription

A

C-MYC

32
Q

contribution of MAD in transcription

A

combine with MAX to turn off transcription and is therefore a tumor-suppressor gene

33
Q

function of Cyclins

A

work to activate CDKs

34
Q

METHODS OF ACTIVATION OF ONCOGENES

A

Point mutations
Chromosomal rearrangements
Gene Amplification

35
Q

Gene emplification is associated with ____ in neuroblastoma and _____ in breast cancer

A

N-MYC in neuroblastoma and C-ERB 2 in breast cancer

36
Q

Tumor suppressor genes work through similar mechanisms as proto-oncogenes through

A

Signal transduction
Cell surface receptors
Nuclear transcription regulators

37
Q

A protein exclusive to the nucleus, is the most common transformed gene in human cancer, presenting in over 50% of human tumors

A

p53

38
Q

action of p53 in the nucleus

A

it stops replication of damaged cells

39
Q

function of p53 after cell damage

A

p53 gets rapidly up regulated and its accumulation triggers increased transcription of DNA repair proteins and those that stop the cell cycle

40
Q

Other tumor suppressor genes include

A

NF-1, NF-2, VHL, and WT-1

41
Q

Function of BCL-2

A

inhibits apoptosis and is transformed in most B cell lymphomas

42
Q

why defective DNA repair genes implicated in development of cancers

A

they may allow cell division despite mutated DNA

43
Q

illustrates a cancer associated with defects in DNA repair

A

HNPCC (hereditary nonpolyposis colon cancer)

44
Q

2 categories of initiators

A

Direct-acting agents

Indirect-acting agents

45
Q

Induction of certain irreversible changes (mutations) in the genome

A

Initiation

46
Q

carcinogenic product of metabolism is called

A

ultimate carcinogen

47
Q

Process of tumor induction in previously initiated cells

A

Promotion

48
Q

how does ionizing radiation induce DNA mutations

A

generation of free radicals from water or oxygen

49
Q

mechanism of ionizing radiation

A

Ionization of macromolecules
Free radical formation
Activation of latent oncogenic viruses
Regenerative replication

50
Q

Epstein - Barr virus (EBV)

A

Burkitt lymphoma

o Nasopharyngeal CA

51
Q

Hepatitis B virus (HBV)

A

Hepatocarcinoma

52
Q

Human Herpesvirus 8 (HHV 8)

A

Kaposi’s sarcoma

53
Q

Human Papillomavirus – 16 (HPV-16)

A

Cervical CA

54
Q

General effects of UV rays

A

Inhibition of cell division
Inactivation of enzymes
Killing of cells

55
Q

Damagae to DNA by UV rays occurs through

A

formation of pyrimidine dimers

56
Q

H pylori causes

A

adenocarcinoma and gastric lymphomas

57
Q

Bacterial cause of gastric malignancies

A

H. pylori

58
Q

First bacterium classified as a carcinogen

A

H. pylori

59
Q

Oncogenic RNA viruses example:

A

Human T-cell lymphotropic virus type I (HTLV-1)

60
Q

Types of Chemical carcinogeneis

A

Direct acting
Procarcinogenesis
Aromatic amines/azo dyes
Naturally-occurring

Pathology (10 decks)

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