Molecular basis of cancer Flashcards

1
Q

what does DNA have

A

bases

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

what do bases fo

A

code the RNA and protein

this affects the cells

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

changes in DNA sequence…

A

If you get a change in DNA, can lead to change in mRNA then change in tRNA, then change sequence of protein (change in aa sequence)

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

what can DNA mutations lead to

A

changes in levels or function of the gene products

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

How is t RNA produced

A

1) DNA unwinds
2) mRNA produced
3) mRNA translocates into cytoplasm
4) Acts as a template at the ribosome
5) forms a sequence with tRNA

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

types of mutation

A

point
gene amplification
chromosomal translocations

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

point mutations

A

single base change

change aa

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

results of point mutations

A

framshift

  • can introduce STOP codon
  • change splicing
  • silent mutations(no aa change)
  • can lose base, moving entire sequence up (change in codon onwards)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

introduction of STOP codon

A

leads to a truncated protein, either does not work or has an altered function

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

change splicing

A

mRNA needs to be spliced to remove introns, mutations in splice sites can either leave introns in or alter the sequence, generally stops production of protein

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

gene amlification

A
  • whole regions of DNA copied more times than they should be
  • normally only one gene, when the DNA copies itself can accidently copy the gene several times
  • each gene will act normally and express itself, therefore there will be an overexpression
  • sends lots of signals to the nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

chromosomal translocations

A
  • movement of whole chromosomes
  • bits of one chromosome can swap with another part
  • The pairs of chromosomes should be the same
  • swap between chromosome regions can lead to eg a receptor to express at different levels
  • affects how cell behaves and divides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

somatic mutations

A
occur in non germline tissues
non heritable
can occur anywhere
accumulate mutations in life
- mutations can occur in the wrong part, genome causes worse changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

gremlin mutations

A

present in sperm and egg
heritable
cause cancer family syndrome

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

de novo

A

can have history of germ mitations

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

characteristics of cancer cells

A
  • excess proliferation without external stimuli
  • loss of control mechanisms
  • loss of apoptosis
  • defects in DNA
  • irreversible, limitless change
  • acquisition of a blood supply into the tumour– angiogenesis
  • invasion of surrounding structures
17
Q

gees involved in cancer

A

oncogenes
tumour suppressor genes
apoptosis genes
mismatch repair genes

18
Q

oncogenes

A
  • apply the accelerator to cell proliferation
  • promote autonomous cell growth and proliferation (no external signal prompts this proliferation in cancer)
  • code for growth factors and their receptors signal transducers and cell cycle components
  • normal function in controlling cell proliferation and cell division balance (proto oncogenes in normal cells, oncogenes in cancer cells)
  • increased expression (activation)or activity in malignancy
19
Q

tumour suppressor genes

A
  • apply brakes to cell proliferation
  • code for factors which control the cell cycle, regulate apoptosis, transcription or cell interactions
  • normal function in supressing cell proliferation and maintaining tissue integrity
  • loss of expression (gene deletion) or function (mutations) in malignancy
20
Q

apoptosis genes

A
  • Genes that regulate normal cell death
    may see
  • increased activity of a gene which inhibits apoptosis
  • reduced activity of genes which promote apoptosis
21
Q

which gene is overexpressed In lymphomas

A

BCL2

apoptosis gene

22
Q

mismatch reapir genes

A
  • code for enzymes important for the repair of damaged DNA
  • DNA damage common due to environmental carcinogens
  • loss of expression (deletion) or function (mutation) in malignancy
  • loss of repair mechanisms increases risk of mutations and activations or loss of oncogenes and tumour suppressor genes
  • allows mutations to accumulate
23
Q

what is proliferation

A

several rounds of cell divisio

24
Q

two hit hypothesis

A
Hit 1
-	inherited loss of gene on one chromosome (germline mutation)
Hit 2
-	sporadic loss on second chromosome
leads to cancer
25
Q

factors in carcinogenesisi

A

genetic (mutations)
environmental (e.g. UV)
chemcials (e.g. tobacco)
viruses

26
Q

multistage carcinogenesis

A

Generally takes a lot of hits to allow the development of cancer
- cells will heal themselves generally
- until they cannot heal themselves, continuing to be exposed to factrs
(multiple genetic events from precancerous to cancer)

27
Q

bowel carcinogenesis

A
normal
hyperplastic
adenoma
carcinoman
metastasis
28
Q

epigenetic

A

doesnt involve changes to DNA bases but alters DNA

  • chemical changes to DNA
  • often occur because of environmental factors age ect
  • increasingly thought to be important in cancer
  • DNA methylation
  • changes to histones
29
Q

tumour microenvironment

A

contribution of other cells surrounding the tumir

all talk to the tumour