Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

// > Cancer Genetics > Flashcards

Cancer Genetics Flashcards

1
Q

What do all cancers result from?

A

Result from changes in the DNA sequences of our genome (these changes occur throughout life because the genome within our cells has been exposed to mutagens like UV radiation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of disease are all cancers?

A

Genetic diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A mutation in what type of gene causes cancer?

A

Cancer gene (mutation alters the function of cancer genes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List some factors that can cause cancer

A

Chemicals (e.g. from smoking) and radiation from environment can damage genes [ENVIRONMENT]

Viruses can introduce their own genes into cells [EXOGENOUS factors]

Heredity, alteration in genes that make a person more susceptible to cancer [GENETICS]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What types of cancer has eating a large amount of fried or barbecued meat been linked to?

A

Increased risk of colorectal, pancreatic and prostate cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a benign tumour and give a common example?

A

Mass of well-differentiated cells that grow slowly, is capsulated and lacks the ability to invade neighbouring tissue or metastasise

e.g. skin moles or uterine fibroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a malignant tumour?

A

Cells are poorly differentiated and capable of invading into adjacent tissues and may be capable of spreading to distant tissues (metastases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can a malignancy be detected?

A

Doctor can take sample of cells via biopsy

Biopsy is analysed under a microscope by a pathologist

If sample shows multiple cells with atypical morphology it may be categorised as malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do cancer cells look like under a microscope?

A

Abnormally large shaped nuclei

Disorganised arrangement

Cytoplasm may also display abnormality such as invaginations

Large nucleus to cytoplasm ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What form the structural basis of the nuclear pore?

A

Nuclearporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does an increase in the number of nuclear pores lead to in advanced cancer?

A

Abnormal influx of beta-cotinine onto the nucleus

beta-cotinine - important transcription factor that is often mutated in colorectal cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are lymphomas?

A

Cancers of the immune system that arise in lymph nodes and tissues of the body’s immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are leukaemia’s?

A

cancers of the immature blood cells that grow in the bone marrow and tend to accumulate in large numbers in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are carcinomas?

A

most common types of cancer arising from cells that cover external and internal body surfaces. Lung, breast and colon are the most frequent cancers of this type (epithelial)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are sarcomas?

A

cancers arising from cells found in the supporting tissues of the body such as the bone, cartilage, fat, connective tissue and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of cancer accounts for the most number of cancer death in the UK?

A

Lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the most common cancers in young people?

A

Leukaemia, ALL, AML, germ cell tumours (testicular cancer), brain tumours (glioma and medulloblastoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 6 hallmarks of cancer?

A

Evading apoptosis

Insensitivity to anti-growth signals

Sustained angiogenesis

Limitless replicative potential

Tissue invasion and metastasis

Self-sufficiency in growth signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does the lifetime risk of developing cancer in a particular tissue correlate with?

A

How often stem cells divide in that tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 2 emerging cancer hallmarks?

A

Dis-regulated metabolism

Evading the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are somatic cells?

A

All cells that form building blocks of the body other than gametes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the difference between germline and somatic mutations?

A

Germline are present in egg or sperm whereas somatic occur in non-germline tissues.

Germline is heritable and rare whereas somatic are non-heritable and very common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Can somatic cells undergo cell division via meiosis and mitosis?

A

NO, they can only divide via mitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of mutation is the most common cause of cancer?

A

Somatic mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why are somatic mutations non-heritable?

A

Because they only occur in somatic cells and not gametes. Only germline mutation in gametes can be passed onto offspring

26
Q

Name a mutation in which gene leads to an increased risk for breast cancer as a part of hereditary breast ovarian cancer syndrome?

A

BRCA-1 gene

27
Q

List the different types of mutation

A

Deletions

Duplications

Inversions

Translocations

Single base mutations (point mutations - silent, nonsense, missense)

28
Q

What does ‘chromosomal instability’ refer to?

A

Higher than normal rate of mis-segregation of chromosomes or part of the chromosomes

29
Q

Is one single mutation enough to give rise to a cancer cell?

A

No

accumulation of mutations involving oncogenes, TSG and DNA repair genes

30
Q

What 3 steps can multi-step carcinogenesis be divided into?

A

Initiation - results from an irreversible genetic alteration. Most likely it is a simple mutation in a tumour suppressor gene

Promotion - excessive cell proliferation and subsequent accumulation of other mutations

Progression - tumour becomes a carcinoma and progress to metastasise in an event

31
Q

What does 1 mega base equate to?

A

1 million bases

32
Q

What does DNA damage from UV radiation lead to?

A

Formation of covalent bonds between 2 adjacent pyrimidines (CC,TC,CT or TT) in the DNA molecules

33
Q

What is the signature mutation of UV light?

A

C to T transition dipyrimidine context

34
Q

What does ‘passenger mutation’ refer to?

A

Mutations that provide no proliferative benefit

many mutations can be tolerated by somatic cells (often in heterozygote state)

35
Q

What does ‘driver mutation’ refer to?

A

Confer a selective advantage to somatic cells in their microenvironment (in homozygote state)

36
Q

What are oncogenes defined as?

A

Cancer genes in which driver mutations are activating or resulting in new functions

most cancer-causing mutations involving oncogenes are acquired, NOT inherited

37
Q

What are oncogenes generally activated by?

A
  1. Chromosome rearrangements
  2. Gene amplification
  3. Mutation
38
Q

What are tumour suppressor genes defined as in terms of ‘driver mutations’?

A

Cancer genes in which driver mutations are inactivating the function

39
Q

When may a passenger mutation be associated with clonal expansion?

A

When they occur in the same genomes, carrying a driver mutation

40
Q

Are most cancer causing mutations involving oncogenes acquired or inherited?

A

Acquired (mainly in somatic cells and very rarely inherited through the germline)

41
Q

What specific chromosomal abnormality is associated with CML?

A

(Reciprocal) Translocation between chromosome 9 and 22, which create an elongated chromosome 9 and truncated chromosome 22

Fuses BCR and ABL

42
Q

What is Myc?

A

Potential transcription factor acting as a proto-oncogene

43
Q

What cellular processes does Ras protein control?

A

Growth, migration, adhesion, cytoskeleton integrity, survival and differentiation

44
Q

When Ras protein is mutated what happens?

A

Cell proliferation is disrupted and the cell start to divide in an uncontrolled manner

45
Q

What is the specific Ras oncogene that is mutated?

A

k-Ras

46
Q

What is the activity of Ras governed by?

A

Its binding to GTP in the active state

Or to GDP in its inactive state

47
Q

What is a tumour suppressor gene (TSG)?

A

A gene that regulates a cell during cell division and replication

48
Q

What happens when a TSG is mutated?

A

Results in a loss or reduction of its function and in combination with other genetic mutation or with the loss of a second allele, it could allow the cells to grow abnormally

Loss of functions of these genes is often recessive

49
Q

What was the first tumour suppressor protein discovered?

A

Retinoblastoma protein Rb, in human retinoblastoma (cancer of the retina)

50
Q

Explain the two-hit hypothesis

A

In the first event there is an inherited mutation, however inheriting one germline copy of a damaged gene present in every cell in the body is not sufficient to enable this cancer to develop

A second hit to the good copy in the gene pair could occur somatically, producing cancer

51
Q

Give one function of retinoblastoma and explain how it carries out this function

A

Prevents excessive cell growth by inhibiting cell cycle progression until a cell has made all checks necessary in G1 phase

52
Q

What phosphorylates retinoblastoma leading to its inactivation?

A

Cyclin dependent kinase

53
Q

Retinoblastoma belong to the pocket protein family whose members have a pocket in the structure for the functional binding of other proteins. What binds to the pocket in retinoblastoma?

A

E2F (important transcription factor essential for activation of the transcription programme of a cell moving onto S phase from G1)

54
Q

What gene encodes the TSG p53?

A

TP53

55
Q

In what syndrome can abnormality of the p53 gene be inherited?

A

Li-Fraumeni syndrome; abnormality can increase the risk of developing various types of cancer

56
Q

What is the overall function of p53?

A

To bind DNA and regulate gene expression to prevent the accumulation of mutations in the genome

57
Q

Genetic variations in which genes increases the risk of breast cancers?

A

BRCA1 and BRCA2

58
Q

Explain the roles of BRCA1 and BRCA2 in DNA repair?

A

BRCA1 is phosphorylated by ATM and CHK2 in response to breaks in double-stranded DNA.

BRCA1 binds to BRCA2 which interacts with RAD51 to form a complex which is involved in DNA repair

59
Q

What virus is responsible for 99% of cervical cancer?

A

HPV (human papilloma virus) (However, not every viral infection leads to cancer and most HPV infections are lower risk and produce a localised disturbance)

60
Q

Which HPV proteins confer a selective growth advantage to the host cells by interfering with the normal function of retinoblastoma and p53?

A

E6 and E7

61
Q

What 3 possible states can a cell that has accumulated a large amount of DNA, or one that no longer effectively repairs damage incurred to its DNA enter into?

A

An irreversible state of dormancy

Cell suicide, AKA apoptosis (programmed cell death)

Unregulated cell division, which can lead to the formation of a tumour that is cancerous

// (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions