carcinogenesis Flashcards

(37 cards)

1
Q

It is a phenomenon of gene alteration, which may result from the interaction of ultimate carcinogens with DNA in the target cell.

A

Initiation

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2
Q

It refers to a phenomenon of gene activation in which the latent altered phenotype of the initiated cell becomes expressed through selection and clonal expansion

A

promotion

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3
Q

It refers to a phenomenon of gene activation in which the latent altered phenotype of the initiated cell becomes expressed through selection and clonal expansion

A

promotion

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4
Q

It is the last irreversible stage of multistage carcinogenesis, which usually develops from the cells in the stage of promotion.

A

Progression

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5
Q

A chemical is transformed into a DNA-reactive metabolite (ultimate carcinogen).

A

Metabolic Conversion to an Ultimate Carcinogen

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6
Q

The ultimate carcinogen binds to DNA, causing structural damage (e.g., mutations, adducts).

A

DNA Interaction and Structural Alteration

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7
Q

Cellular repair mechanisms may reverse the damage, but if unsuccessful, mutations persist.

A

DNA Repair Attempts

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8
Q

When the damaged cell divides, the mutation becomes permanently fixed in the genome

A

Cell Proliferation and Mutation Fixation

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9
Q

It is the second stage in multistage carcinogenesis, characterized by the activation of gene expression that leads to the clonal expansion of initiated cells.

Unlike initiation, promotion does not involve direct DNA damage but rather alters gene expression patterns, allowing preneoplastic cells to proliferate

A

PROMOTION

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10
Q

ASPECTS OF PROMOTION

A

Reversible
Non Genotoxic
Long Duration
Dose Dependent

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11
Q

Dependent on continuous exposure to promoting agents; lesions may regress if
exposure stops.

A

Reversible

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12
Q

Tumor promoters do not directly damage DNA but modify cellular signaling pathways

A

Non Genotoxic

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13
Q

Can persist for decades in humans.

A

Long Duration

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14
Q

Exhibits threshold effects (sigmoid dose-response curve)

A

Dose-Dependent

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15
Q

Promoters stimulate the proliferation of initiated cells, giving them a growth advantage.

A

Clonal Expansion of Initiated Cells

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16
Q

Promoters modify cell signaling pathways, leading to changes in:
-Growth factors (e.g., EGFR signaling).
-Anti-apoptotic mechanisms (e.g., Bcl-2 upregulation).
-Inflammatory responses (e.g., NF-κB activation

A

Altered Gene Expression

18
Q

Many promoters (e.g., phenobarbital, TCDD) suppress programmed cell death, allowing
preneoplastic cells to survive.

A

Inhibition of Apoptosis

19
Q

Withdrawal of promoters can lead to apoptosis-induced regression of preneoplastic
lesions.

A

Reversibility and Regression

20
Q

It represents the final, irreversible stage of multistage carcinogenesis,
developing from previously promoted cells. This stage is characterized by
increasing genomic instability and karyotypic evolution, leading to morphologically
detectable changes in cellular structure.

21
Q

Key Aspects of Progression

A

Irreversible genetic damage (distinct from reversible promotion)
Karyotypic instability (abnormal chromosome structure/number)
Emergence of invasive/metastatic potential
Clinical cancer manifestation

22
Q

Chemicals that drive transition from promotion to progression

A

Progressor Agents

23
Q

The dose of a substance that causes death in 50% of a population of test animals.

A

LD50 (Lethal Dose 50):

24
Q

The concentration of a substance in the environment that causes death in 50% of a
population of test organisms.

A

LC50 (Lethal Concentration 50):

25
The highest dose or concentration of a substance that does not cause any observable adverse effects
NOAEL (No Observed Adverse Effect Level)
26
The highest concentration of a substance that does not cause any observable effects.
NOEC (No Observed Effect Concentration):
27
The lowest concentration of a substance that causes observable effects
LOEC (Lowest Observed Effect Concentration)
28
are the methods used to determine the harmful effects of substances on living organisms.
Toxicity measurements
29
are the specific effects or outcomes that are measured in toxicity tests, such as lethality, growth, reproduction, or changes in behavior or physiology
Toxicity endpoints
30
Short-term tests measuring the effects of high concentrations of chemicals, with endpoints often reflecting lethality.
Acute Toxicity Tests
31
Longer-term tests measuring the effects of lower, less toxic concentrations, with endpoints concerning sublethal effects like reproduction or grow
Chronic Toxicity Tests
32
It is the first critical stage in chemical carcinogenesis, characterized by permanent genetic damage in a target cell due to exposure to a carcinogenic agent.
INITIATION
33
Activates PKC → cell proliferation
TPA (Phorbol ester)
34
Induces liver enzyme activity → cell growth
Phenobarbital
35
Binds Ah receptor → alters gene expression
TCDD (Dioxin)
36
Promotes colon cell proliferation
Colic Acid
37
Cigarette smoke contains initiators (e.g.,) and promoters (e.g.,)
benzo(a)pyrene phenols