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EXMD 504 Biology of Cancer > Chromosomal Aberrations in Cancer > Flashcards

Chromosomal Aberrations in Cancer Flashcards

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1
Q

What is the order of the formation of the nucleus, from smallest to largest structure?

A

Chromatin -> histones -> nucleosomes -> chromatosome -> chromatid -> chromosome

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2
Q

Chromosomes are organized in _______________ in the nucleus

A

Territories

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3
Q

Active genes are located at the ____________ of the domains, while silenced genes are located in the ____________

A

Surface; interior

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4
Q

Alternatively, closed chromatin domains with ___________ genes are transformed into an __________ configuration before transcriptional activation

A

Silenced; open

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5
Q

What are the phases of mitosis?

A

Interphase, prophase, metaphase, anaphase, telophase

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6
Q

Link the following molecular activities to the stage of mitosis:
a) Chromosome periphery assembly
b) Surface stiffening to nuclear envelope assembly
c) Sister chromatid resolution
d) Sister chromatid separation

A

a) Prophase
b) Telophase
c) Interphase
d) Anaphase

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7
Q

At which stage of mitosis are condensin I and II needed?

A

Prophase to telophase

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8
Q

At which stage of mitosis is BAF needed?

A

Interphase and telophase

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9
Q

Propagation of the genetic information to ____________ cells is tightly controlled through the cell _________

A

Daughter; cycle

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10
Q

Associate the following factors with the following checkpoints:
a) Cycle arrest
b) Promoting cell cycle progression
c) DDR (DNA damage response) pathway

A

a) Wee1
b) CDK, cyclin
c) TopBP1

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11
Q

Place the following events of SAC activation in order:
a) Recruitment of regulators BUBR1, BUB3, CDC20 and MAD2
b) No ubiquitination and degradation of cyclin B1 and securin
c) Inactivation of the APC/C
d) Cell arrested in mitosis
e) Unattached kinetochores

A

e, a, c, b, d

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12
Q

Place the following events of SAC activation in order:
a) Accurate attachment of chromosomes to microtubule spindles
b) Ubiquitination of securin and cyclin B1
c) Inactivation of SAC
d) Release of separase
e) Separation of sister chromatids
f) Cleavage and opening of cohesion ring
g) CDC20 binding and activation of the APC/C

A

a, c, g, b, d, f, e

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13
Q

Boveri suggested that aberrant mitoses led to the ____________ distribution of chromosomes

A

Unequal

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14
Q

Boveri suggested that tumors might arise because of abnormal _________________ of chromosomes in daughter cells

A

Segregation

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15
Q

The Philadelphia chromosome results from reciprocal translocation between which chromosomes?

A

9 and 22

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16
Q

How does the Philadelphia chromosome cause chronic myeloid leukemia?

A

The fusion of ABL1 gene from chromosome 9 and BCR gene from chromosome 22

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17
Q

How much time does the chronic phase last?

A

5-6 years

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18
Q

How much time does the accelerated phase last?

A

6-9 months

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19
Q

How much time does the blast crisis last?

A

3-6 months

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20
Q

What technique was used to get a better definition of chromosomal alteration found in leukemic cells?

A

Refined cytogenetic technique

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21
Q

There are more cases of CML in older generations than younger generations

A

False, there are less cases of CML in older generations than younger generations

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22
Q

What is the drug that is used to help patients with CML?

A

Imatinib

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23
Q

At the time of resistance of imatinib, what proportion of patients are found to carry mutations in the BCR-ABL1 kinase domain?

A

30-70%

24
Q

What are other examples of chromosomal imbalances?

A

Monosomy, trisomy

25
Q

Chromosomal rearrangements that disrupt transcription factor genes can result in what?

A

Fusion proteins with enhanced or aberrant transcriptional activity or that mediate transcription repression

26
Q

Deregulated expression of normal genes can lead to which diseases?

A

Burkitt’s lymphoma, acute myeloid leukemia, prostate cancer

27
Q

Which one of the following is NOT a group of sarcomas?
a) Fusion driven sarcomas
b) Non-translocation-associated sarcomas of intermediate genomic complexity
c) Sarcomas with sarcomas balanced karyotypes

A

c)

28
Q

True or false: Fusion driven sarcomas arise de novo and harbour multiple defining cytogenetic abnormalities that are present at initiation and retained throughout their clonal evolution

A

False, they harbour a single defining cytogenetic abnormality that is present at initiation and retained throughout their clonal evolution

29
Q

What do the majority of gene fusions resulting from the translocations encode?

A

Chimeric transcription factors that cause the transcriptional dysregulation of target genes

30
Q

Which of the following is NOT a theme in driven sarcomas?
a) The fusion gene creates a constitutively active form of an RTK activating proliferation/survival pathways
b) The fusion gene enables an autocrine mechanism that feeds the tumor through specific growth factors
c) The fusion gene has a p53 domain

A

c)

31
Q

Which domain is lost in the PAX3-FOXO1 fusion?

A

DNA-binding domain of FOXO1 and transactivation domain of PAX3

32
Q

Ewing sarcoma is the translocation of which chromosomes?

A

EWS on chromosome 22 and FLI1 on chromosome 11

33
Q

Which types of sarcoma are driven by chromosome 12 amplifications, often manifesting as double minute chromosomes and ring chromosomes?

A

Well-differentiated and dedifferentiated liposarcomas

34
Q

Which oncogenes can serve as confirmatory diagnostic markers for non-translocation associated sarcomas?

A

CDK4 and MDM2

35
Q

True or false: Sarcomas with complex karyotypes show aneuploidy and complex cytogenetic changes that lack specificity

A

True

36
Q

What are some examples of sarcomas with complex karyotypes?

A

Osteosarcoma, undifferentiated pleomorphic sarcomas

37
Q

Which tumor suppressors are involved in sarcomas with complex karyotypes?

A

TP53 and RB1

38
Q

Osteosarcoma (OS) is defined as a tumor forming an _______________ bone matrix called an ___________

A

Immature; osteoid

39
Q

Osteosarcoma accounts for what percent of all bone tumors?

A

20%

40
Q

What is the pattern of hypermutation associated with SVs in half of the OS?

A

Kataegis

41
Q

How do genomic rearrangements happen in cancer?

A

DNA sequence and chromatin features, inappropriate DNA repair or recombination, cellular stress and spatial proximity

42
Q

What contributes intratumor heterogeneity?

A

Karyotypic diversity within the cancer cell population from CIN

43
Q

True or false: The tumors must develop CIN-tolerance mechanisms in order to propagate

A

True

44
Q

True or false: TP53 loss of function leads to aneuploidy

A

False, TP53 loss of function is necessary for stable loss of aneuploidy and establishment of CIN

45
Q

Which of the following mechanisms do NOT act through TP53?
a) Casp2 loss
b) p21 gain
c) PIK3CA mutations
d) Hippo pathway

A

b)

46
Q

Which of the following attenuates the effects of CIN?
a) APC/C dysfunction allows segregation error correction and prevents excessive CIN
b) Transition to near-diploid karyotypes enhances cancer cell fitness

A

a)

47
Q

The balance between _______ and tolerance mechanisms define the overall tumor ____________

A

CIN; fitness

48
Q

What would result from a cell with sustainable level of CIN and tolerance of W-CIN and S-CIN?

A

Mostly cells with complex karyotype restrained by multiple tolerance pathways

49
Q

All connective tissues originate from embryonic ______________

A

Mesenchyme

50
Q

Which of the following is not a characteristic of mesenchymal cells?
a) Prominent nucleoli
b) Round-shaped
c) Undifferentiated

A

b)

51
Q

What does mesenchyme produce?

A

Stem cells for tissues like blood, muscle and vascular endothelium

52
Q

What are the two major groups of sarcomas?

A

Soft tissue and bone sarcomas

53
Q

Who do sarcomas affect the most?

A

Children, adolescents and young adults

54
Q

Molecular profiling is used to detect what?

A

New entities in tumors and reunite entities that were previously thought to be distinct

55
Q

Sarcomas can be defined by their _____________ alterations, while most epithelial tumors are defined by the _______ of origin

A

Molecular; organ

56
Q
A

EXMD 504 Biology of Cancer (5 decks)

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