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Pathology Midterms > Neoplasia: Molecular Basis Of Cancer > Flashcards

Neoplasia: Molecular Basis Of Cancer Flashcards

1
Q

Acquired mutations caused by

A 
Exogenous agents (viruses, chemicals)
Endogenous of cellular metabolism
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2
Q

Principal targets of cancer causing mutations

A

Growth promoting proto oncogenes
Growth inhibiting tumor suppressor genes
Genes that regulate programmed cell death
Genes involved in DNA repair

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3
Q

Growth promoting proto oncogenes

A

Gain of functions
Excessive function
Complete new function
Dominant in normal cells

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4
Q

Tumor suppressor genes

A

Loss of function

Both genes must be damaged in most

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5
Q

Only one gene damaged but still it caused tumor suppressor genes

A

Haploid insufficiency

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6
Q

Apoptosis

A

Less death that enhances survival a of cells

Gain of function - suppress apoptosis
Loss of function - promote cell death

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7
Q

DNA repair

A

Loss of function

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8
Q

Contribute to the development of malignant phenoyptype

A

Driver mutations

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9
Q

First driver mutation

A

Initiating mutations

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10
Q

Ang mga iniated cells ay mag acquire ng? Nag mag co contribute sa development ng cancer at ito ay matagal

A

Additional driver mutations

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11
Q

Cancers arise from cells with stem cell like properties

A

Cancer stem cells

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12
Q

Common early step on the road to malignancy

A

Loss of function mutations

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13
Q

Increase the frequency of mutations but no phenotypic consequences

A

Passenger mutations

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14
Q

More common than driver mutations

A

Passenger mutations

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15
Q

Competition among tumor cells for access to nutrient and micro environmental riches

A

Darwinian contest or selection

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16
Q

Pernicious tendency of tumors to become more aggressive over time

A

Tumor progression

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17
Q

Two types of mutation in DNA sequencing

A

Present in all tumor site

Unique to a subset of tumor sites

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18
Q

Present in the founding cell at the moment of transformation

A

Present in all tumor site

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19
Q

Unique to a subset of tumor sites

A

During after the transformation
During outgrowth and spread of tumor
Family trees
Galápagos Islands

20
Q

Explain natural history of cancer

Changes in tumor behavior therapy

A

Selection of the fittest cells

21
Q

Selective pressures that cancer cells face

A

Chemotherapy or radiotherapy

22
Q

Pero pag nag recur ang tumor resistant na ito sa chemotherapy

A

Nice to know

23
Q

Also contribute to the malignant properties of cancer cells. Except DNA mutations

A

Epigenetic aberrations

24
Q

Epigenetic aberrations includes

A

DNA methylation

Histone modifications

25
Q

Silence gene expression

A

DNA. Methylation

26
Q

Enhance dampen gene expression

A

Histone modifications

27
Q

Unlike DNA mutations, Epigenetic are

A

Potentially reversible by drugs

28
Q

DNA mutations

Epigenetic

A

Passed to daughter cells

29
Q

DNA methylation

A

Silencing effect

30
Q

Histone modification

A

Far ranging effects

31
Q

Cellular and molecular hallmarks of cancer

Oncogene activation

A

Self sufficiency in growth signals

32
Q

Inactivation of tumor suppressor gene

A

Insensitivity to growth inhibitory signals

33
Q

Warburgs effects

A

Altered cellular metabolism

34
Q

Metabolic switch to aerobic glycolysis

For rapid cell growth

A

Warburg effects

35
Q

Resistant to programmed cell death

A

Evasion apoptosis

36
Q

Immortality

Stem cell like property

A

Limitless replicative potential

37
Q

Kahit walang vascular supply

A

Sustained angiogenesis

38
Q

Accelerated those hallmarks of cancer

A

Genomic instability

Cancer promoting inflammation

39
Q

Genes that promotes autonomous cell growth in cancer cells

A

Oncogenes

40
Q

Un mutated cellular counter part of oncogene

A

Proto oncogene

41
Q

Encode proteins by oncogene

Freed from normal checkpoints

A

Oncoproteins

42
Q

Most frequently mutated oncogenic pathway

A

Tyrosine kinase pathway

43
Q

Accelerators of DNA replication

A

Once proteins

44
Q

Slow or brakes

A

Tumor suppressors

45
Q

Physiologic conditions of growth factor

A
  1. Growth factor bind ps to receptor
  2. Activate cytoplasmic signal transducing proteins
  3. Transmits to nucleus via: cytoplasmic receptor proteins or 2nd messenger
  4. DNA transcription
  5. Cell division
46
Q

Nonlethal genetic damage lies at the heart of

A

Carcinogenesis

Pathology Midterms (5 decks)

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