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Pathology > Carcinogenesis > Flashcards

Carcinogenesis Flashcards

1
Q

Four classes of normal regulatory genes?

A
  1. Growth-promoting proto-oncogenes, 2. Growth-inhibiting tumor suppressor genes, 3. Genes that regulate programmed cell death (i.e.,
    apoptosis) , 4. Genes involved in DNA repair
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2
Q

Consid­ered dominant because mutation of a single allele
can lead to cellular transformation

A

Growth-promoting proto-oncogenes

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3
Q

Usually both normal alleles of tumor suppressor genes must be
damaged for transformation to occur.

A

Tumor suppressor genes

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4
Q

May act like proto-­oncogenes (loss of one copy is

sufficient) or tumor suppressor genes (loss of both copies).

A

Genes that regulate apoptosis and DNA repair

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5
Q

needs growth factors to proliferate ?

A

Normal cell

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6
Q

How normal cell reacts to growth factors?

A

Growth factor (GF) binds to its receptor (GFR) – GFR activation results in several cytoplasmic signal
transduction molecules which transfers signals to nucleus – Activation of several nuclear regulatory factors that
initiates DNA transcription resulting in cell proliferation

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7
Q

have the capacity to proliferate without external stimuli, which usually occurs as a consequence of oncogene activation.

A

Tumors

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8
Q

Normal cellular genes whose products promote cell proliferation

A

Proto-oncogenes:

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9
Q

Mutant proto-oncogenes that function autonomously without a requirement for normal growth-promoting signals.

A

Oncogenes

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10
Q

Oncogenes they can work at the level of?

A

1/Growth Factors, 2/Growth Factor receptors, 3/Cytoplasmic proteins involved in signaling, 4/ Nuclear regulatory proteins 5/ Cell
cycle regulators.

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11
Q

Examples of oncogenes?

A

AMPLIFICATION & OVEREXPRESSION / MUTATION

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12
Q

Examples of oncogenes,

A

AMPLIFICATION & OVEREXPRESSION / MUTATION

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13
Q

Examples of oncogenes/ AMPLIFICATION & OVEREXPRESSION ?

A

HER2

(growth factor receptor) in breast carcinoma

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14
Q

Examples of oncogene/ MUTATION?

A

EGFR (epidermal growth factor receptor)
mutation in lung adenocarcinoma resulting in constitutional
activation of receptor

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15
Q

encode proteins that inhibit cellular proliferation by

regulating the cell cycle. ?

A

Tumor suppressor

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16
Q

which code for proteins involved in regulating the
cell cycle, repairing damaged DNA or, if the DNA is damaged beyond repair,
inducing programmed cell death ( apoptosis ) ?

A

Tumor suppressor genes

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17
Q

Failure of tumor suppressor gene function leads to?

A

failure of growth inhibition which is characteristic of tumors

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18
Q

Governor of the Cell Cycle

?

A

RB Gene:

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19
Q

exerts anti proliferative effects by controlling the G1- to-S
transition of the cell cycle ?

A

Rb

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20
Q

Almost all cancers have a disabled G1checkpoint due to

?

A

mutation of RB genes

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21
Q

Guardian of the Genome?

A

TP53 Gene

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22
Q

central monitor of stress in the cell • Can be activated by DNA damage.

A

p53 protein

23
Q

controls the expression and activity of genes involved

in cell cycle arrest, DNA repair, cellular senescence, and apoptosis. ?

A

Activated p53

24
Q

Eg of Tumor suppressor genes?

A

RB Gene/ TP53 Gene

25
Q

functions to prevent
propagation of malignant cells by stimulation of apoptosis and
cell cycle arrest in affected cells
?

A

P53

26
Q

Exposure to carcinogens and mutagens in normal cells (normal

53) results in?

A

DNA damage by stimulation of apoptosis or cell

cycle arrest to allow DNA repair.

27
Q

Exposure to carcinogens and mutagens in cells with mutant

non functioning 53 results?

A

expansion of affected cells

28
Q

Evasion of Cell Death

A

The balance between pro-apoptotic (e.g., BAX,
BAK) and anti-apoptotic molecules (BCL2, BCL-XL).
• In 85% of follicular B cell lymphomas, the anti-apoptotic gene
BCL2 is activated by the t(14;18) translocation.

29
Q

Normal cells after certain numbers of divisions reach?

A

terminally

non-dividing (replicative senescence)

30
Q

How cells count number of divisions?

A

Unknown but possibly by shortening of “telomeres” at the end
of each chromosome, which when shortened beyond certain
point leads to stimulation of P53-dependent cell cycle arrest

31
Q

Germ cells?

Dividing

A

They have enzyme (telomerase) leads to cell’s sustained

ability to replicate

32
Q

Cancer cells replication by?

A

By acquiring telomerase activity (detected in over

90% of tumors), this gives the malignant cell a stem-cell like features

33
Q

caused by defects in DNA mismatch repair genes

?

A

Familial colon carcinoma as well as endometrial and ovarian

carcinoma

34
Q

process through which new blood vessels form from

pre-existing vessels

A

Angiogenesis

35
Q

produced by

tumor cells is the main growth factor responsible for Angiogenesis?

A

Vascular Endothelial Growth Factor [VEGF]

36
Q

Ability to invade tissues, occurs in four steps: ?

A
  1. Loosening of cell–cell contacts :
  2. Degradation of ECM,
  3. Attachment to novel ECM components,
  4. Migration of tumor cells.
37
Q

Cell–cell contacts are lost by the inactivation of

A

E-cadherin

38
Q

Basement membrane and interstitial matrix degradation is

mediated by?

A

proteolytic enzymes secreted by tumor cells and

stromal cells.

39
Q

Migration/motility of tumor cells by ?

A

tumor-derived cytokines”

motility factor”.

40
Q

Patients with HNPCC syndrome (Hereditary Non-Polyposis

Colorectal Cancer) have defects in?

A

mismatch repair system, leading to development of carcinomas of the colon.

41
Q

Patients with xeroderma pigmentosum :increased risk for the

development of cancers of the?

A

skin exposed to UV light.

42
Q

process which results in the transformation of normal cell
to neoplastic cell by causing genetic alterations and cumulative
genetic defects

A

Carcinogenesis

43
Q

is an agent that participates in causing the tumor, its
ultimate site of action is mainly DNA
?

A

Carcinogen

44
Q

causing hepatocellular carcinma ?

A

HBV

45
Q

causing lung cancer

?

A

Tobacco

46
Q

Over a period of time, many tumors become more
aggressive and acquire greater malignant potential & less
responsive to therapy ?

A

tumor progression

47
Q

Carcinogens types?

A

1) Chemical Carcinogens (2) Radiation Carcinogens (3) Microbial Carcinogens

48
Q

Chemicals?

A

ALKYLATING AGENTS / ACYLATING/AROMATIC AMINES, AMIDES, AZO DYES /Chemotherapy drugs (e.g., alkylating agents) : leukemia.

49
Q 
Chemotherapy drugs (e.g., alkylating agents) : leukemia.
?
A

Chemicals carcinogen

50
Q

Therapeutic irradiation of the head and neck can give rise to ?

A

thyroid cancers years later.

51
Q

Skin cancers (melanomas, squamous cell carcinomas, and
basal cell carcinomas). • Fair­ skinned people. • Melanomas are associated with intense intermittent
exposure, as occurs with sunbathing
From?

A

UV radiation

52
Q

human papilloma virus (HPV),

/ HBV ?

A

2.Oncogenic DNA Viruses e

53
Q

3.Helicobacter pylori, is implicated in the?

A

genesis of both gastric

adenocarcinomas and gastric lymphomas.

Pathology (8 decks)

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