phase 1 week 4 Flashcards Preview

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Flashcards in phase 1 week 4 Deck (95):
1

What is a tumour?

A tumour is formed by an excessive, uncontrolled proliferation of cells as a result of irreversible genetic change which is passed from one tumour cell to its progeny

2

What is cancer?

A neoplastic disease of which the natural course of which is (often) fatal

3

For epithelial tumours what is the normal way in which cells change to become cancerous?

normal > dysplasia > benign > pre-malignant > malignant

4

What is dysplasia?

"Bad growth" - loss of architectural orientation and development of cellular atypic. Cannot yet invade neighbouring tissue so is not cancer

5

What is metaplasia?

cells change from one differentiated tissue to another. Unstable environment so high chance of mutations in DNA - precursor to dysplasia and cancer

6

What are some modes of cancer spread?

local invasion
lymphatic spread
blood spread
transcolaemic spread

7

What do proto-oncogenes do?

Code for proteins that are needed for normal cell proliferation

8

What is a oncogene?

a mutated proto-ongogene

9

what are activating mutations?

only certain mutations in a proto-oncogene will convert it to the oncogenic form

10

What does the activation of proto-oncogenes do?

allows cells to bypass the need for extracellular growth signals

11

Why are porto-oncogenes described as dominant acting?

only one allele of a photo-oncogene needs to be acquire an activating mutation

12

What do oncogenes code for?

a hyperactive version of a protein product
or
normal protein BUT
in abnormal quantities
at the wrong time
in the wrong cell type

13

What mutations can lead do hyperactive proteins being formed?

point mutation - e.g ras Ki-ras in colon cancer
deletion
chromosomal rearrangement e.g. ber-able in CML

14

What mutations can cause proteins to be formed in the wrong place, time or amount?

gene amplification (HER2) breast cancer
Chromosomal rearrangement - places gene downstream of a promoter e.g lg-myc

15

What external signals for growth be mutated to lead to cancer?

hormones
peptide growth factors

16

Give examples of cell surface receptors that can be mutated

HER2
EGFR

17

Give examples of intracellular molecules that can be mutated?

signal transducers (ras)
cyclins (cyclin D)
transcription factors (myc)

18

What can constitutive telomerase expression do?

hay flick limit not reached so the cell is immortalised

19

What is a benign tumour?

stay localised at their site of origin

20

What is a malignant tumour?

able to invade and spread to different sites

21

What are the b and m endings for epithelial tumours?

oma and carcinoma

22

what are the b and m names for covering epithelium tissues?

papilloma and carconoma

23

what are the b and m names for glandular epithelial tumours?

adenoma, adenocarcinoma

24

What are the b and m names for tumours in the epithelium forming organs (e.g. liver)

adenoma
carcinoma e.g. hepatocarcinoma

25

What are the b and m endings for connective tissue tumours?

oma
sarcoma

26

what are the b and m names for smooth muscle tumours?

leiomyoma
leiomyosarcoma

27

what are the b and m names for skeletal muscle tumours?

rhabdomyoma
rhabdomyosarcoma

28

what are the b and m names for bone forming tumours?

osteoma
osteosarcoma

29

what are the b and m names for cartilage tumours

chondroma
chondrosarcoma

30

what are the b and m names for fibrous tumours?

fibroma
fibrosarcoma

31

what are the b and m names for tumours of blood vessels

angioma
angiosarcoma

32

what are the b and m names for adipose tissue tumours?

lipoma
liposarcoma

33

what are the b and m names for lymphoid tumours?

n/a
lymphoma

34

what are the b and m names for haematopoetic tumours?

n/a
leukaemia

35

what are the b and m names fir primitive nerve cell tumours?

n/a
neuroblastoma e.g. retinoblastoma

36

what are the b and m names fir glial cell tumours?

n/a
glioma e.g. astrocytoma

37

what are the b and m names for tumours in melanocytes?

pigmented naevi
malignant melanoma

38

what are the b and m names for tumours in the mesothelium?

n/a
malignant mesothelioma

39

what are the b and m names for tumours in germ cells

teratoma
teratoma, seminoma

40

How do tumours get an adequate nutrient supply once they are larger than 1-2mm?

secrete VEGF (vascular endothelial growth factor)
promotes production of new vascular tubules

41

what are MMPs?

matrix metalloproteinases (chew up basement membrane)

42

what is uPA?

urokinase plasminogen activator

43

What are some risk factors for cancer?

age
alcohol
cancer-causing substances
chronic inflammation
diet
hormones
immunosuppression
infectious agents
obesity
radiation
sunlight
tobacco

44

what happens during G1?

growth in mass, centrosome duplication

45

what happens during s phase?

chromosome duplication - synthesis of DNA

46

what happens during G2?

cell grows in size, duplicating organelles and preparing for division

47

what happens during cytokinesis?

cleavage of daughter cells

48

what are the 5 stages of mitosis?

prophase
pro-metaphase
metaphase
anaphase
telophase

49

what happens during prophase?

chromatin condensation
nucleolus disappears
centrioles move to the poles of the cell

50

what happens during pro-metaphase?

nuclear membrane dissolves
chromosomes attach to microtubules and begin moving

51

What happens during metaphase?

spindle fibres align the chromosomes along the middle of the cell nucleus (metaphase plate)

52

What happens during anaphase?

paired chromosomes separate and move to opposite sides of the cell

53

What happens during telophase?

chromatids arrive at opposite poles of the cell
new membranes form around the daughter nuclei
chromosomes decondense
spindle fibres disperse

54

What are cyclin-dependent kinases?

serine / threonine kinases that require the binding of cyclin for full activity
regulate progression through the cell cycle
activity must be tightly regulated
waves of expression of specific cyclins
phosphorylation / dephosphorylation

55

What are cyclins?

activator proteins that are up - or down - regulated depending on the phase of the cell cycle

56

What are cyclin-dependent kinase inhibitors?

small proteins that block cdk/cyclin activity either by forming an inactive complex or acting as a competitive CDK ligand

57

What is the cyclin / cdk complex needed at the end of G1?

CDK4/6 - cyclin D

58

What is the cyclin / cdk complex needed for progression through mitosis?

CDK1 - cyclin B

59

What is CDK1 - cyclin B also known as?

maturation promoting factor (MPF)

60

What are the four well established check points in the cell cycle?

restriction point (G1)
DNA damage check points (end of G1 and G2)
Metaphase check point

61

What is cell cycle progression dependent on?

growth factors

62

the accumulation of which cyclin means that no growth factors are required for the rest of the cell cycle and that cell is committed to cell division?

cyclin D

63

What acts as the gate keeper at the restriction point?

retinoblastoma (RB)

64

What is the function of p53?

cellular stress e.g. DNA damage leads to transcription of p53
at low levels this results in p21 expression which arrests the cell cycle and allows time for the DNA to be repaired
at high levels it promotes apoptosis of the cell

65

What are the benefits and limitations of X-rays?

good for bones
chest X-ray
abdomen limited

66

What are the benefits and limitations of CT scans?

excellent for bones
chest and abdomen
25 seconds
limited for soft tissues of spine, limbs and brain

67

What are the benefits and limitations of MRI?

great for brain, spine soft tissues, limbs
less good for abdomen / pelvis
no good for heart or lungs
25 minutes

68

What is CT?

A modern imaging tool that combines X-rays with computer technology to produce a more detailed, cross-sectional view of the body

69

How does an MRI work?

Magnetic field around the patient
pulses radio waves
radio waves cause tissues to resonate
a computer measures the rate at which various tissues give of vibrations and converts it into a 2D picture

70

What are the 3 main stages of life before birth?

pre-implantation
embryonic stage
foetal stage

71

When is the pre-implantation stage?

week 1

72

When is the embryonic stage and what does it involve?

weeks 2-8
organogenesis

73

When is the foetal stage and what does it involve?

weeks 9-38
growth and development

74

Describe cleavage

mitotic divisions of fertilised oocyte
overall size remains the same
allows passage down narrowest part of the uterine tube (isthmus)
surrounded by a glycoprotein coat - zona pellucida - to prevent premature implantation

75

Describe morula formation

around day 4, cells maximise contact with each other
a cluster of cells forms held together by tight junctions
enters the uterus

76

Describe blastocyst formation

first sign of cellular differentiation
inner cell mass - goes on to form embryo and extra-embryonic tissues
outer cells form trophoblast - contributes to placenta
fluid enters via the zona pellucida into the spaces of the inner cell mass
A fluid-filled blastocyst cavity forms

77

What causes the blastocyst to "hatch"

ICM cells undergo proliferation and fluid builds up in cavity
eventually blastocyst "hatches" from the zona pellucida to facilitate implantation

78

What happens in week 2?

implantation

79

what days does implantation occur?

7-12

80

Which cells implant first?

trophoblast

81

What does the trophoblast differentiate into?

cytotrophoblast
syncytotrophoblast

82

what makes up the bilaminal disk?

the epiblast and the hypoblast

83

Describe the amnion

continuous with the epiblast
persists until birth
cavity fills with amniotic fluid
protection for developing embryo

84

Describe the yolk sac

continuous with the hypoblast
important for nutrient transfer in weeks 2-3
disappears around week 20

85

Describe the chorion

trophoblast and extra embryonic mesoderm
forms foetal component of placenta
chorionic cavity seen early in pregnancy disappears when amnion expands

86

What is gastrulation?

a process of cell division and migration resulting in the formation of three germ layers

87

What are the three germ layers?

ectoderm
mesoderm
endoderm

88

Describe the formation of the three germ alters

once the cells have invaginated, some displace the hypoblast creating the endoderm and others between the epiblast and the newly created endoderm form the mesoderm
the remaining cells in the epiblast form the ectoderm
the cells in these layers give rise to all tissues and organs in the embryo

89

Describe gap junction communication

sieve like structure at plasma membranes of opposing cells
hemi-channels composed of connexin molecules
Hemi-Channels of one cell align with those of another
physical sharing of ions and small cytoplasmic molecules
cells behave as a syncytium

90

What is endocrine signalling?

long range (blood)
e.g. oestrogen

91

What is paracrine signalling?

local - neighbouring cells (via diffusion)
e.g. epidermal growth factor

92

What is autocrine signalling?

same cell
insulin-like growth factor 1

93

what is juxtracrine signalling?

signal adjacent to receptor
e.g. laminin

94

What is intracrine signalling?

signal produced in cell acts on nuclear or internalised receptor
e.g. fibroblast growth factor 11

95

How do steroids work?

diffuse across plasma membrane
bind directly to intracellular receptors
hormone-receptor complex acts as a transcription factor
Affects gene expression directly