WK14: Molecular Oncology Flashcards

1
Q

6 Hallmarks of Cancer

A
  • Self-sufficiency in growth signals
  • Insensitivity in anti-growth signals
  • Tissue invasion and metastasis
  • Limitless replicative potential
  • Sustained angiogenesis
  • Evading apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cancer characteristics

A
  • Clonality
  • Autonomy
  • Anaplasia
  • Metastasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

In clonality genetic disease is at the _______ level

A

cellular (mutations have a critical role)

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

A proliferating mass of cells lead to ______ formation

A

tumor

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

What consequence of genetic instability is associated with mutations in offspring

A

Phenotypic Heterogeneity

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

Promote/ Accelerate cell proliferation

A

oncogenes

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

only 1 of a pair of oncogenes needed to be activated for it to express _____ _______

A

malignancy potential (dominant and highly conserved)

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

off state of oncogene

A

proto-oncogene

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

Inhibit growth and multiplication of mutated cells

A

TS (tumor suppressor genes)

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

True or False:

TS genes are dominant and highly conserved

A

False (recessive)

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

Cell adhesion molecules

A

APC, DCC

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

Regulators of cell cycle

A

RB1, Tp53

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

Matching Type:
1st HIT
2nd HIT

a. Gross chromosomal loss
b. TS mutation or inherited mutation

A

1st HIT - b

2nd HIT - a

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

Gene involved in sporadic mutation

A

Wild-Type TS Gene

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

Familial type of TS gene defects

A

Heritable Cancer Syndromes

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

True or False:
In Heritable Cancer Syndromes, there is a tendency to develop malignancy at an earlier age compared to wild-type mutations because 1st hit is already present at birth

A

True

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

Ensures fidelity of replication

A

DNA repair genes

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

increased propensity of oncogenes and TS genes to undergo mutation is called ________

A

Microsatellite Instability/MIN

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

areas of unstable DNA because mutations are already present there

A

MIN

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

Inhibits cell cycle progression & permits DNA repair to take place

A

P21

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

most common genetic alteration found in human cancer

A

P53

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

True or False:

anti-apoptotic = favors continuous proliferation of tumor cells

A

True

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

main mechanism of lymphoid tumors is overexpression of _____

A

BCL-2

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

Component of mitochondria released in response to apoptotic signals

A

Cytochrome C

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

Activates cascade resulting in DNA fragmentation and apoptosis

A

Executioner/Effector Caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

two types of caspases

A

Initiator Caspases

Executioner/Effector Caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Prevent recombination and shortening of the lagging strand

A

telomeres

28
Q

The telomere is a bio/repro clock which regulate amount of ______ in a cell

A

replications

29
Q

Adds 6 nucleotide repeats to 3’-OH end of DNA

A

telomerase

30
Q

Commonly used to define DNA sequence changes that alter protein function

A

Mutations

31
Q

Occur in non-germline tissues

A

somatic mutation

32
Q

____ _____ are heritable – causes cancer family syndrome and Mendelian cancer syndrome

A

Germline mutation

33
Q

True or False:

In germline mutation, all cells are affected in offspring; risk is present at birth

A

True

34
Q

Approximately _____% of breast, ovarian, and colon cancers are linked to hereditary risks

A

5-10%

35
Q

Clinical features of Hereditary Cancer Syndrome

A
  • 2 or more relatives in a family is diagnosed with cancer
  • > 1 gen is affected
  • 1 or more types of clustering of specific tumor types are present
36
Q

Common in tissues with rapid turnover

A

Autonomy

37
Q

mean length of time for division of all tumor cells present

A

doubling time

38
Q

True or False

The growth of cancer is directly proportional to rate of progression and aggressiveness of tumor

A

True

39
Q

LOW number of cells, circulating factors, and nutrients in the tumor bed

A

Lag Phase

40
Q

Rapid proliferation phase

A

Log Phase

41
Q

Tumors in the _______ phase tend to be resistant to

chemotherapy and radiotherapy

A

plateau

42
Q

earliest time for cancer to be clinically detected

A

Junction between lag and log phases

43
Q

Only phase of the cell cycle that is susceptible to manipulation by external agents

A

S-phase

44
Q

if promoted by cyclin → cell goes into mitosis

A

Junction between G2 and M

45
Q

commonly affected in many malignancies

A

Junction between G1 and S

46
Q

Therapeutic goal in this phase: is the prevention of mitosis in the presence of damaged DNA

A

G2/M checkpoint

47
Q

Area most often involved in cancer

A

G1/S checkpoint

48
Q

Phosphorylation of Rb gene results in:

A

Activation of several genes needed for S phase progression

Promotes differentiation through association with
transcription factors

49
Q

caused by Rb gene mutation

A

Retinoblastoma

50
Q

True or False:
The more poorly differentiated the tumor is, the more anaplastic it tends to be, the
more aggressive the behavior of the tumor is

A

true

51
Q

Continued proliferation results in mass formation

A

anaplasia

52
Q

lifestyle related causes of malignancy

A

Tobacco, Diet , Sexual practices

53
Q

The most carcinogenic substance ever produced by human

beings for commercial consumption

A

Tobacco

54
Q

2nd most common carcinogenic substance produced by human beings for commercial consumption

A

Alcohol

55
Q

The higher the caloric intake, the higher intake of red meat = the higher the chance of developing ______

A

colon cancer

56
Q

The use of _______ in post-menopausal women to alleviate the post-menopausal symptoms can increase the development of breast cancer

A

estrogens

57
Q

Ionizing radiation includes: ______ ____ and _______ ______

A

electromagnetic rays & particulate matter

58
Q

Exposure to radiation from sunlight can cause a high risk of ____ _____ and ______

A

skin cancer and melanoma

59
Q

Most RNA oncogenic viruses belong to the family of retroviruses that contain ______ _____

A

reverse transcriptase

60
Q

Many patients with gastric cancers have history of ________

A

chronic peptic ulcer disease

61
Q

_____ and tissue cytology usually for masses that are hard to access like lung and liver masses

A

FNAB

62
Q

Useful for identifying the primary site of tumor if the patient already presents with metastasis

A

Cytokeratin phenotyping

63
Q

_____ is diagnostic for non-seminomatous germ cell tumors

A

AFP

64
Q

Can provide baseline information In staging, certain blood examinations are necessary such as functional assessment of end organs

A

Serum chemistries

65
Q

main site of activation and deactivation of chemotherapeutic agents

A

Liver function test

66
Q

______ insufficiency can lead to prolonged activation or prolonged deactivation which leads to toxicity

A

Hepatic