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EXMD 504 Biology of Cancer > Aberrant gene expression in cancer biology > Flashcards

Aberrant gene expression in cancer biology Flashcards

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1
Q

Aberrant gene expression can be driven by specific genomic and _______________ alterations

A

Epigenomic

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2
Q

True or false: Different cell types are programmed to express different sets of genes, but they all have the same DNA

A

True

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3
Q

Epigenetics covers all phenomena that produces _____________ changes in genome _______________ that do not affect the DNA sequence

A

Heritable; function

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4
Q

The expression state of a gene is determined by what factors?

A

The packaging or accessibility of its DNA regulatory regions
The presence of transcription factors and chromatin modifying enzymes

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5
Q

The nucleosome is made of a histone ____________ with 2 subunits for each histone

A

Octomer

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6
Q

What are the four histones?

A

H2A, H2B, H3 and H4

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7
Q

Associate the following descriptions to the enzymes of post-translational epigenetic modifications
i. Proteins that read histone modifications
ii. Remove post-translational modifications
iii. Chromatin-remodeling proteins that move nucleosomes and allow gene transcription
iv. Add modifications

A

i. Readers
ii. Erasers
iii. Movers
iv. Writers

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8
Q

Epigenetic modifications like the _____________ of lysines can determine ____________ elements across the genome

A

Acetylation; functional

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9
Q

ChIP-Seq is used to map the location of ____________ associated with the chromatin across the genome

A

Proteins

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10
Q

Genes can be identified based on their _______________ in the epigenome

A

Expression

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11
Q

The chromatin is organized in _________

A

3D

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12
Q

Topologically associated domains (TADs) are regions that loop and are _____________ from each other

A

Separate

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13
Q

Which method is used to observe the open chromatin?

A

ATAC-Seq (Assay for Transposase-accessible chromatin using sequencing)

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14
Q

ATAC-Seq demonstrates the regions where ____________ elements can transpose in the open chromatin

A

Transposable

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15
Q

Chromatin ______________ profiles reveal distinct molecular subtypes of cancers

A

Accessibility

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16
Q

What is the goal of precision oncology?

A

Cancer diagnosis, prognosis, prevention and/or treatment targeted to the needs of the patients

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17
Q

Which protein was targeted for therapy for melanoma?

A

BRAF

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17
Q

What method was used to observe the treatment of melanoma?

A

FDG-PET

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18
Q

What treatment was used on patients with melanoma carrying the V600E BRAF mutation?

A

BRAF inhibitor PLX4032

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18
Q

Oncogenes are ___________ acting cancer genes that are activated by ___________-of-function mutations

A

Dominantly; gain

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19
Q

Tumor suppressors are __________ acting cancer genes that are activated by ___________-of-function mutations

A

Recessively; loss

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20
Q

Cancers are characterized by ____________ mutations

A

Somatic

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21
Q

____________ mutations are positively selected and important for cancer development

A

Driver

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22
Q

Some driver mutations can be inherited in the _______________

A

Germline

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23
Q

Mutations are typically _____________ and do not exceed ______________% allelic frequency

A

Heterozygous; 50

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24
Q

How are cancer driver genes identified?

A

Recurrent somatic mutations

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25
Q

How do oncogenes and tumor suppressors differ?

A

Distribution of cancer-associated mutations

26
Q

IDH1/2 cancer-associated mutations are specific _____________ mutations

A

Missense

27
Q

What method is used to detect DNA copy number variation?

A

DNA sequencing of the tumor and normal copy

28
Q

Copy number ___________ can be incorporated into the genome

A

Gains

29
Q

Many high-level amplifications in cancer occur on circular ______________ DNA

A

Extrachromosomal

30
Q

True or false: There is no centromeric activity in ecDNA

A

True

31
Q

Circular ecDNA is associated with _________ outcome

A

Poor

32
Q

DNA sequencing can help in looking for oncogenes in recurrent copy number _________ and tumor suppressors in recurrent copy number __________

A

Gain; loss

33
Q

What percent of human cancers harbour mutations/alterations in chromatin-related proteins?

A

50%

34
Q

Which of the following do malignant cells exhibit?
i. Chromatin structure
ii. Deranged developmental programs
iii. Non-regulatory element activity

A

i and ii

35
Q

Mutations in histone H3.3 occur at three residues. What are they?

A

K27, K36 and G34

35
Q

What did the paper “Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma” identify?

A

Recurrent mutations in histone proteins at specific lysine sites that were modified

36
Q

H3.3-K27M and H3.3-K36M mutations are dominant _____________ and _____________ the genome-wide methylation of H3K27 and H3K36

A

Negative; reduce

36
Q

H3.3-G34R and H3.3-G34V mutations reduce the levels of __________ on the same or nearby nucleosomes

A

H3K36me3

37
Q

True or false: Histone modifying enzymes can also have alterations

A

True

37
Q

Which histone modifying enzyme is most commonly mutated?

A

Mover

38
Q

What percent of all cancers harbour mutations in SWI/SNF-encoding genes?

A

20%

39
Q

How many different genes encoding subunits of the SWI/SNF family of chromatin remodelling complexes are recurrently mutated?

A

Nine

39
Q

The tumor suppressor activity in mutations in chromatin remodelling complexes is attributable to their roles in facilitating ____________ ____________ function

A

Transcription factor

39
Q

SWI/SNF complex is _____________ to PRC complex

A

Antagonist

39
Q

What is the most commonly mutated protein across almost all cancers?

A

P53

39
Q

The majority of the genome is __________

A

Noncoding

40
Q

True or false: Noncoding mutations do not lead to aberrant expression of oncogenes

A

False, they can lead to aberrant gene expression and expression of oncogenes

40
Q

The larger fraction of somatic mutations are found in the ______________

A

Heterochromatin

41
Q

True or false: Noncoding regulatory elements harbour more somatic mutations than coding reulatory elements

A

True

41
Q

Highly recurrent mutations in human melanoma are found in the _________ promoter

A

TERT

41
Q

Can noncoding mutations drive cancer?

A

Yes

41
Q

Can TERT promoter mutations modulate transcription factor binding to chromatin?

A

Yes

42
Q

Noncoding ___________ outside of oncogenes are selectively amplified with or without their respective oncogenes

A

Enhancers

42
Q

True or false: Identifying driver mutations is harder in noncoding regions than coding regions

A

True

42
Q

What is another type of noncoding driver mutation?

A

Noncoding RNA

43
Q

Do all CNVs target the gene within them?

A

No

43
Q

Enhancers selectively amplified without their respective oncogenes are more like ___________

A

Duplications

44
Q

What can explain aberrant gene expression patterns?

A

Enhancer hijacking events

44
Q

Copy number alterations can affect the activation of which protein?

A

GFI1

45
Q

Expression of __________ is activated from the duplication of SNCAIP

A

PRDM6

45
Q

What can expose additional enhancer hijacking events?

A

Epigenetic profiling

46
Q

SNCAIP duplication is highly recurrent in which group of medulloblastoma?

A

Group 4

47
Q

Which of the following are examples of enhancer hijacking?
i. Intrachromosomal inversion
ii. Extrachromosomal deletion
iii. Enhancer duplication
iv. Insulator deletion

A

i, iii, iv

47
Q

___________ enables distal DNA interactions

A

ecDNA

48
Q

Interplay between the ___________ and the _____________ drives aberrant gene expression in cancer

A

Genome; epigenome

EXMD 504 Biology of Cancer (11 decks)

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