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Module 2 > Oncogenesis and Neoplasia > Flashcards

Oncogenesis and Neoplasia Flashcards

1
Q

What are the cell cycle stages

A

G0
G1 - cell grows to full size
S - DNA synthesis
G2 - rapid cell contents productions
M - cell division
Cytokinesis

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2
Q

What does G1 checkpoint check for

A

nutrients
growth factors
DNA damage

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3
Q

What does G2 checkpoint check for

A

cell size
DNA replication

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4
Q

What does metaphase checkpoint check for

A

chromosome spindle attachment

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5
Q

why are cyclins degraded

A

avoid uncontrolled chain reactions

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6
Q

When do CDKs become active

A

bound to cyclins

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7
Q

What is the action of cyclin/CDK

A

phosphorylate Rb
Rb changes in conformation
RB uncouples from E2F
E2F acts as a TF for S phase gene transcription

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8
Q

Types of genes which are mutated in cancer

A

proto-oncogenes
oncogenes
tumour suppressor genes

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9
Q

What are proto oncogenes

A

genes that possess normal gene products and stimulate normal cell development
e.g. GF (C-Myc and K-Ras)

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10
Q

How do oncogenes form

A

gain of function mutation of protooncogenes

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11
Q

What are oncogenes

A

more active than normal or active at inappropriate times and stimulate unregulated cell proliferation

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12
Q

What is a tumour suppressor gene

A

gene that’s normal function is to constrain cell proliferation and partial or complete inactivation lead to an increased likelihood of cancer development
e.g. p53 and Rb
loss of function can cause cancer

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13
Q

When is p53 activated

A

DNA damage
cell cycle abnormalities
hypoxia

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14
Q

What is the function of normal p53

A

apoptosis
cell cycle arrest
DNA repair
cell cycle restart

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15
Q

mutant p53

A

present in >50% of all cancers, inhibits self removal of the mutant cells, prolongs propagation and proliferation

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16
Q

Two groups associated with tumorigenesis

A

gain of function - inappropriate activation of oncogenes
loss of function - inactivation of tumour suppressor genes

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17
Q

what are common properties of cancer cells

A

-resisting cell death
-sustaining proliferative signalling
-evading growth suppressors
-activating invasion and metastasis
-enabling replicative immortality
-inducing angiogenesis

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18
Q

What are the 6 steps of cancer diagnosis/progression defined at the molecular level

A
  1. self sufficiency of growth (overproducing GFs)
  2. do not respond to usual growth inhibitory signals e.g. cell cycle cycle checkpoints
  3. evasion of apoptotic mechanisms e.g. p53 mutations
  4. immortalisation e.g. loss of telomere shortening
  5. neoangiogenesis e.g. overproduction of VEGF for new vessels
  6. invasion and metastasis e.g. alterations in production of cellular adhesion molecules
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19
Q

What are the hallmarks of cancer

A

emerging: deregulating cellular energetics and avoiding immune destruction
enabling characteristics: genome instability and tumour promoting inflammation

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20
Q

point mutations

A

change in an individual base pair of a DNA sequence
e.g. p53 and k-Ras mutations

21
Q

What occurs in avain leukosis virus (ALV)

A

viral genome integrates into the host genome and uses its trong promoter and enhancer sequences to alter the expression of nearby genes (c-Myc), inducing tumours

22
Q

Example of translocation

A

Burkitt’s lymphoma
translocation between chromosome 8 and 14
c-Myc under the control for the antibody heavy chain gene (CH)
high expression of c-myc and excessive cell division causing cancer

23
Q

How long does a multi-step process take

A

years

24
Q

Example of knudson 2 hit hypothesis

A

retinoblastoma - childhood cancer of the eye
hereditary (40% in both eyes) - one mutation is inherited (silent), second hit in retinal cells

sporadic (60% in one eye) - 2 hits in same eye in somatic tissue

25
Q

vogelstein’s model of colorectal carcinogenesis

A

Chromosome 5q APC mutation
DNA hypomethylation
Chr 12p K-Ras mutation
Chr 18q DCC loss
Chr 17p TP53 loss
other alterations

26
Q

Ras-Raf-MAPK pathway

A
  1. GF binding
  2. conformational change in shape
  3. adapter protein phosphorylated
  4. Ras activated
  5. MEK phosphorylation
  6. stimulates cell growth
  7. MAPK activated
27
Q

cancer initiators

A

chemical carcinogens
viruses
radiation
BRCA mutation
unknown factors

28
Q

cancer promoters

A

inflammation
hormones
normal growth promoters

29
Q

example of occupational cancers

A

asbestos increases the chances of mesothelioma

30
Q

alcohol related cancers

A

-cancer of the mouth and oesophagus
-head and neck cancer
-bowel cancer
-liver cancer
-pancreatic cancer
-breast cancer

31
Q

where is cancer common due to UV exposure

A

australia
NZ

32
Q

Virus related cancers

A

Hep B - Liver
Hep C - Liver
HPV - Uterine cervix
EBV - Burkitt’s lymphoma/nasopharynx, Hogdkin’s disease

33
Q

microorganism related cancer

A

Helicobacter pylori - stomach
Schistosoma haematobrium - urinary bladder

34
Q

Iatrogenic agents

A

ionizing radiation - breast/lung/leukemia
chemotherapy - bone marrow
immunosupressive drugs
exogenous hormones - breast

35
Q

What is hyperplasia

A

excessive number of cells

36
Q

what is metaplasia

A

normal cells of one differentiated type displaced by another type of differentiated cells

37
Q

What is dysplasia

A

cytologically abnormal cells
-variability in nucleus size and shape
-increased nuclear staining
-increased ratio of nuclear vs cytoplasmic size
-increased mitotic activity
-lack of cytoplasmic features

38
Q

Benign or Malignant

A

1) degree of differentiation/anaplasia
2) rate of growth
3) local invasion
4) metastasis

39
Q

degree of differentiation/anaplasia

A

Benign - well differentiated, few mitosis
Malignant - well differentiated to undifferentiated (anaplasia)

40
Q

more rapid growth =

A

less differentiated

41
Q

rate of growth

A

Benign tumours - slow
malignant tumours - quick

42
Q

local invasion

A

benign tumours are rarely invasive and delineated by a fibrous capsule
malignant tumours - infiltration of surrounding tissue and invasion to adjacent via breaching of basement membrane
if pre-invasive (within basement membrane) - carcinoma in situ

43
Q

Metastasis

A

benign tumours do not metastasise - compress adjacent tissue
malignant tumours locally invade and travel to the blood/lymph to establish secondary tumours

44
Q

grading of tumours

A

-differentiation
-pleiomorphism
mitotic index

45
Q

staging of tumours

A

TNM

46
Q

T

A

tumour
T0 = breast free of tumour
T1 = lesion <2cm
T2 = lesion 2-5cm
T3 = skin/chest wall involved by invasion

47
Q

N

A

nodes
N0 = no axillary nodes involved
N1 = mobile nodes involved
N2 = fixed nodes involved

48
Q

M

A

metastasis
M0= no metastases
M1 = demonstrable metastases
MX = suspected metastases

Module 2 (7 decks)

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